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1.
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue ; 36(5): 514-519, 2024 May.
Artigo em Chinês | MEDLINE | ID: mdl-38845499

RESUMO

OBJECTIVE: To investigate the effect of mild hypothermia on macrophage polarization in lipopolysaccharide (LPS)-induced acute lung injury (ALI) mice and to clarify its role in lung injury. METHODS: According to a random number table method, 18 male C57BL/6 mice were divided into sham operation group (Sham group), ALI normothermic model group (NT group) and ALI mild hypothermia treatment group (HT group), with 6 mice in each group. The ALI model in mice was established by the method of tracheal instillation of LPS, and temperature control was administered at 1 hour after surgery. The anus temperature in NT group was kept at 36-38?centigrade, while the anus temperature in HT group was kept at 32-34?centigrade. The target anus temperature in both groups were maintained for 6 hours and then slowly rewarmed to 36-38 centigrade. The Sham group was infused with an equal amount of physiological saline through the trachea without temperature control. After 24 hours of modeling, serum was collected and mice were sacrificed to obtain lung tissue. Pathological changes in lung tissue were observed under light microscopy and semi-quantitative lung injury score was performed. Enzyme linked immunosorbent assay (ELISA) was used to detect the serum levels of interleukins (IL-1ß, IL-10). Real-time quantitative polymerase chain reaction (RT-qPCR) was used to test the indicators of macrophage polarization, such as the mRNA expressions of CD86, IL-6, CD206 and arginase 1 (Arg1) in the lung tissue. The protein expression of M1 macrophage marker inducible nitric oxide synthase (iNOS) and M2 macrophage marker Arg1 were detected by Western blotting. RESULTS: Compared with the Sham group, the NT group appeared significant pulmonary hemorrhage and edema, thickened lung septum, inflammatory cell infiltration, and lung injury score was significantly increased; serum IL-1ß level was significantly elevated; IL-10 level was increased without statistical significance; the expressions of CD86 mRNA, IL-6 mRNA and iNOS protein were significantly elevated, and CD206 mRNA was significantly decreased; the mRNA and protein expressions of Arg1 decreased, but there were no significant differences. Compared with the NT group, the pathological injury of lung tissue in HT group was significantly reduced, and the lung injury score was significantly decreased (4.78±0.96 vs. 8.56±1.98, P < 0.01); serum IL-1ß level was decreased (ng/L: 13.52±1.95 vs. 27.18±3.87, P < 0.01), and IL-10 level was significantly increased (ng/L: 42.59±15.79 vs. 14.62±4.47, P < 0.01); IL-6 mRNA expression was decreased in lung tissue (2-ΔΔCt: 3.37±0.92 vs. 10.04±0.91, P < 0.05), the expression of M1 macrophage markers CD86 mRNA and iNOS protein were significantly decreased [CD86 mRNA (2-ΔΔCt): 0.52±0.16 vs. 1.95±0.33, iNOS protein (iNOS/ß-actin): 0.57±0.19 vs. 1.11±0.27, both P < 0.05], the expression of M2 macrophage markers CD206 mRNA, Arg1 mRNA and Arg1 protein were significantly increased [CD206 mRNA (2-ΔΔCt): 3.99±0.17 vs. 0.34±0.17, Arg1 mRNA (2-ΔΔCt): 2.33±0.73 vs. 0.94±0.23, Arg1 protein (Arg1/ß-actin): 0.96±0.09 vs. 0.31±0.11, all P < 0.05]. CONCLUSIONS: Mild hypothermia can alleviate the inflammatory response and protect lung tissue in ALI mice, which may be related to the inhibition of M1 macrophage polarization and promotion of M2 macrophage polarization.


Assuntos
Lesão Pulmonar Aguda , Lipopolissacarídeos , Macrófagos , Camundongos Endogâmicos C57BL , Animais , Lesão Pulmonar Aguda/terapia , Masculino , Camundongos , Macrófagos/metabolismo , Lipopolissacarídeos/efeitos adversos , Óxido Nítrico Sintase Tipo II/metabolismo , Interleucina-10/metabolismo , Interleucina-6/metabolismo , Hipotermia Induzida , Interleucina-1beta/metabolismo , Modelos Animais de Doenças
2.
Fa Yi Xue Za Zhi ; 40(2): 179-185, 2024 Apr 25.
Artigo em Inglês, Chinês | MEDLINE | ID: mdl-38847034

RESUMO

OBJECTIVES: To detect the expression changes of interleukin-10 (IL-10) and transforming growth factor-ß1 (TGF-ß1) during the development of deep vein thrombosis in mice, and to explore the application value of them in thrombus age estimation. METHODS: The mice in the experimental group were subjected to ligation of inferior vena cava. The mice were sacrificed by excessive anesthesia at 1 d, 3 d, 5 d, 7 d, 10 d, 14 d and 21 d after ligation, respectively. The inferior vena cava segment with thrombosis was extracted below the ligation point. The mice in the control group were not ligated, and the inferior vena cava segment at the same position as the experimental group was extracted. The expression changes of IL-10 and TGF-ß1 were detected by immunohistochemistry (IHC), Western blotting and real-time qPCR. RESULTS: IHC results revealed that IL-10 was mainly expressed in monocytes in thrombosis and TGF-ß1 was mainly expressed in monocytes and fibroblast-like cells in thrombosis. Western blotting and real-time qPCR showed that the relative expression levels of IL-10 and TGF-ß1 in each experimental group were higher than those in the control group. The mRNA and protein levels of IL-10 reached the peak at 7 d and 10 d after ligation, respectively. The mRNA expression level at 7 d after ligation was 4.72±0.15 times that of the control group, and the protein expression level at 10 d after ligation was 7.15±0.28 times that of the control group. The mRNA and protein levels of TGF-ß1 reached the peak at 10 d and 14 d after ligation, respectively. The mRNA expression level at 10 d after ligation was 2.58±0.14 times that of the control group, and the protein expression level at 14 d after ligation was 4.34±0.19 times that of the control group. CONCLUSIONS: The expressions of IL-10 and TGF-ß1 during the evolution of deep vein thrombosis present time-dependent sequential changes, and the expression levels of IL-10 and TGF-ß1 can provide a reference basis for thrombus age estimation.


Assuntos
Modelos Animais de Doenças , Imuno-Histoquímica , Interleucina-10 , Fator de Crescimento Transformador beta1 , Veia Cava Inferior , Trombose Venosa , Animais , Interleucina-10/metabolismo , Interleucina-10/genética , Fator de Crescimento Transformador beta1/metabolismo , Fator de Crescimento Transformador beta1/genética , Trombose Venosa/metabolismo , Trombose Venosa/etiologia , Camundongos , Veia Cava Inferior/metabolismo , Veia Cava Inferior/patologia , Masculino , Fatores de Tempo , Monócitos/metabolismo , Western Blotting , RNA Mensageiro/metabolismo , RNA Mensageiro/genética , Reação em Cadeia da Polimerase em Tempo Real , Ligadura , Fibroblastos/metabolismo
3.
Front Public Health ; 12: 1369675, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38827614

RESUMO

Background: Coronary heart disease (CHD) is the leading cause of death in both developed and many developing countries. Exercise training is a fundamental component of cardiac rehabilitation programs for patients with CHD. This study aims to investigate the effects of a Tai Chi rehabilitation program, which is provided through a hybrid online and offline mode, on oxidative stress and inflammatory responses in patients with CHD. Methods: A total of 34 patients with coronary heart disease were randomly assigned to two groups: an experiment group (n = 14, age 62.07 ± 9.076 years) and a control group (n = 20, age 61.90 ± 9.700 years). The experiment group underwent a 12-week Tai Chi cardiac rehabilitation program (TCCRP), while the control group followed a conventional exercise rehabilitation program (CERP) consisting of 1-h sessions, 3 times per week, for a total of 36 sessions. Participants were studied at baseline and post-intervention. The main assessments include the levels of Malondialdehyde (MDA), Superoxide dismutase (SOD), Tumor necrosis factor (TNF-α) and Interleukin-10 (IL - 10) in blood samples. Pearson correlation analysis was used, and the differences between the two groups were subsequently tested using two-way repeated ANOVA. Statistical significance was defined as a two-sided p-value of <0.05. Results: The key finding of the study reveals that MDA was significantly reduced by 1.027 nmoL/mL. Additionally, the TCCRP showed significant improvements in SOD and IL-10, with values of 10.110 U/mL and 2.441 pg./mL, respectively. Notably, a significant positive correlation was found between SOD and IL-10 (r = 0.689, p = 0.006), while MDA showed a significant positive correlation with TNF-a (r = 0.542, p = 0.045). In contrast, the ECRP group only showed a significant improvement in SOD. Conclusion: The study conducted a 12-week program on TCCRP, which utilized a hybrid online and offline model for individuals with coronary heart disease. The program showed promising results in alleviating oxidative stress and inflammation, possibly by regulating the balance between oxidative and antioxidative factors, as well as pro-inflammatory and anti-inflammatory factors.


Assuntos
Doença das Coronárias , Inflamação , Interleucina-10 , Malondialdeído , Estresse Oxidativo , Tai Chi Chuan , Humanos , Masculino , Pessoa de Meia-Idade , Doença das Coronárias/reabilitação , Feminino , Interleucina-10/sangue , Malondialdeído/sangue , Fator de Necrose Tumoral alfa/sangue , Idoso , Superóxido Dismutase/sangue
4.
Mol Biol Rep ; 51(1): 712, 2024 Jun 01.
Artigo em Inglês | MEDLINE | ID: mdl-38824221

RESUMO

INTRODUCTION: Coronary artery disease (CAD) in young adults can have devastating consequences. The cardiac developmental gene MEIS1 plays important roles in vascular networks and heart development. This gene effects on the regeneration capacity of the heart. Considering role of MEIS1 in cardiac tissue development and the progression of myocardial infarction this study investigated the expression levels of the MEIS1, HIRA, and Myocardin genes in premature CAD patients compared to healthy subjects and evaluated the relationships between these genes and possible inflammatory factors. METHODS AND RESULTS: The study conducted a case-control design involving 35 CAD patients and 35 healthy individuals. Peripheral blood mononuclear cells (PBMCs) were collected, and gene expression analysis was performed using real-time PCR. Compared with control group, the number of PBMCs in the CAD group exhibited greater MEIS1 and HIRA gene expression, with fold changes of 2.45 and 3.6. The expression of MEIS1 exhibited a negative correlation with IL-10 (r= -0.312) expression and positive correlation with Interleukin (IL)-6 (r = 0.415) and tumor necrosis factor (TNF)-α (r = 0.534) gene expression. Moreover, there was an inverse correlation between the gene expression of HIRA and that of IL-10 (r= -0.326), and a positive correlation was revealed between the expression of this gene and that of the IL-6 (r = 0.453) and TNF-α (r = 0.572) genes. CONCLUSION: This research demonstrated a disparity in expression levels of MEIS1, HIRA, and Myocardin, between CAD and healthy subjects. The results showed that, MEIS1 and HIRA play significant roles in regulating the synthesis of proinflammatory cytokines, namely, TNF-α and IL-6.


Assuntos
Doença da Artéria Coronariana , Proteína Meis1 , Proteínas Nucleares , Transativadores , Adulto , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Estudos de Casos e Controles , Proteínas de Ciclo Celular/genética , Proteínas de Ciclo Celular/metabolismo , Doença da Artéria Coronariana/genética , Expressão Gênica/genética , Regulação da Expressão Gênica/genética , Interleucina-10/genética , Interleucina-6/genética , Interleucina-6/metabolismo , Leucócitos Mononucleares/metabolismo , Proteína Meis1/genética , Proteína Meis1/metabolismo , Proteínas Nucleares/genética , Proteínas Nucleares/metabolismo , Transativadores/genética , Transativadores/metabolismo , Fatores de Transcrição/genética , Fatores de Transcrição/metabolismo , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/metabolismo
5.
J Neuroinflammation ; 21(1): 143, 2024 May 31.
Artigo em Inglês | MEDLINE | ID: mdl-38822367

RESUMO

The dysregulation of pro- and anti-inflammatory processes in the brain has been linked to the pathogenesis of major depressive disorder (MDD), although the precise mechanisms remain unclear. In this study, we discovered that microglial conditional knockout of Pdcd4 conferred protection against LPS-induced hyperactivation of microglia and depressive-like behavior in mice. Mechanically, microglial Pdcd4 plays a role in promoting neuroinflammatory responses triggered by LPS by inhibiting Daxx-mediated PPARγ nucleus translocation, leading to the suppression of anti-inflammatory cytokine IL-10 expression. Finally, the antidepressant effect of microglial Pdcd4 knockout under LPS-challenged conditions was abolished by intracerebroventricular injection of the IL-10 neutralizing antibody IL-10Rα. Our study elucidates the distinct involvement of microglial Pdcd4 in neuroinflammation, suggesting its potential as a therapeutic target for neuroinflammation-related depression.


Assuntos
Proteínas Correpressoras , Interleucina-10 , Camundongos Knockout , Microglia , Doenças Neuroinflamatórias , PPAR gama , Transdução de Sinais , Animais , Masculino , Camundongos , Proteínas Adaptadoras de Transdução de Sinal/deficiência , Proteínas Adaptadoras de Transdução de Sinal/genética , Proteínas Adaptadoras de Transdução de Sinal/metabolismo , Proteínas Reguladoras de Apoptose/metabolismo , Proteínas Reguladoras de Apoptose/genética , Proteínas Reguladoras de Apoptose/deficiência , Proteínas Correpressoras/genética , Proteínas Correpressoras/metabolismo , Depressão/metabolismo , Depressão/etiologia , Interleucina-10/metabolismo , Interleucina-10/deficiência , Interleucina-10/genética , Lipopolissacarídeos/toxicidade , Camundongos Endogâmicos C57BL , Microglia/metabolismo , Microglia/efeitos dos fármacos , Chaperonas Moleculares/genética , Chaperonas Moleculares/metabolismo , Doenças Neuroinflamatórias/metabolismo , PPAR gama/metabolismo , PPAR gama/genética , Transdução de Sinais/fisiologia , Transdução de Sinais/efeitos dos fármacos
6.
Neurology ; 102(12): e209527, 2024 Jun 25.
Artigo em Inglês | MEDLINE | ID: mdl-38830184

RESUMO

OBJECTIVES: Despite a high response rate at the first evaluation during induction chemotherapy, the risk of early relapse remains high and unpredictable in primary CNS lymphomas (PCSNLs). We aimed to assess the prognostic value of early IL-10 levels in CSF (e-IL-10) after 2 months of induction chemotherapy. METHODS: We retrospectively selected from the LOC (Lymphomes Oculo-Cérébraux) network database patients with PCSNLs who had complete or partial response at the 2-month evaluation of a high-dose methotrexate-based first-line chemotherapy for whom e-IL-10 was available. RESULTS: Thirty patients (median age: 62 years, brain involvement in 30/30, CSF involvement in 10/30, median baseline CSF IL-10: 27.5 pg/mL) met the selection criteria. e-IL-10 was undetectable in 22 patients and detectable in 8 patients. At the end of induction treatment, 7 of 8 and 4 of 22 of the patients with detectable and undetectable e-IL-10 had experienced progressive disease, respectively (p = 0.001, OR: 26.8, 95% CI 2-1,478). The median progression-free survival times were 5.8 months (95% CI 2.8-8.8) and 28.7 months (95% CI 13.4-43.9) in the groups with detectable and undetectable e-IL-10, respectively (p < 0.001). DISCUSSION: Our results suggest that despite an objective response, the persistence of detectable e-IL-10 is associated with a high risk of early relapse in PCNSL. A closer follow-up of such patients is warranted.


Assuntos
Neoplasias do Sistema Nervoso Central , Quimioterapia de Indução , Interleucina-10 , Humanos , Pessoa de Meia-Idade , Feminino , Masculino , Interleucina-10/líquido cefalorraquidiano , Neoplasias do Sistema Nervoso Central/líquido cefalorraquidiano , Neoplasias do Sistema Nervoso Central/tratamento farmacológico , Idoso , Estudos Retrospectivos , Prognóstico , Adulto , Linfoma/líquido cefalorraquidiano , Linfoma/tratamento farmacológico , Metotrexato/uso terapêutico , Metotrexato/administração & dosagem
8.
Sci Rep ; 14(1): 13196, 2024 06 08.
Artigo em Inglês | MEDLINE | ID: mdl-38851847

RESUMO

Interleukin-10 (IL-10) is an immunomodulatory cytokine that plays a pivotal role in the pathogenesis of acute coronary syndromes (ACS). Here, we evaluated the role of IL10 promoter variants as markers for ACS susceptibility in Western Mexican patients as well as its association with IL10 mRNA and IL-10 plasma levels. Three promoter variants (- 1082 A > G, - 819 T > C and - 592 A > C) were analyzed in 300 ACS patients and 300 control group (CG) individuals. IL10 relative gene expression was evaluated in peripheral blood mononuclear cells (PBMC) and IL-10 levels were quantified in plasma. The allelic, genotypic and haplotypic frequencies did not show significant differences between groups. ACS patients had sevenfold higher mRNA IL10 level compared to CG (p = 0.0013). Homozygous C/C carriers in both - 819 T > C and - 592 A > C variants had 0.4-fold higher IL10 mRNA expression than heterozygous and polymorphic allele homozygous genotypes (p = 0.0357) in ACS group. There were significant differences in plasma IL-10 levels in CG and ACS group (1.001 vs 1.777 pg/mL, p = 0.0051). The variants were not markers of susceptibility to ACS in Western Mexican individuals. ACS patients showed higher IL10 expression than CG individuals which could be mediated by - 819 T > C and - 592 A > C variants and pharmacotherapy.


Assuntos
Síndrome Coronariana Aguda , Predisposição Genética para Doença , Interleucina-10 , Polimorfismo de Nucleotídeo Único , Regiões Promotoras Genéticas , Humanos , Interleucina-10/genética , Interleucina-10/sangue , Síndrome Coronariana Aguda/genética , Síndrome Coronariana Aguda/sangue , Masculino , Feminino , Pessoa de Meia-Idade , Idoso , Estudos de Casos e Controles , Genótipo , Alelos , Biomarcadores/sangue , México , Leucócitos Mononucleares/metabolismo , Frequência do Gene , RNA Mensageiro/genética , RNA Mensageiro/metabolismo
9.
PLoS One ; 19(6): e0292830, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38857232

RESUMO

Lipopolysaccharide (LPS), a component of the Gram-negative bacterial cell wall, activates Toll-like receptors (TLRs). Porphyromonas gingivalis (Pg) may be involved in the progression of periodontal disease. Mice exposed to a novel environment show hyperlocomotion that is inhibited by systemic administration of LPS derived from Escherichia coli (Ec-LPS). However, whether Pg-LPS influences novelty-induced locomotion is unknown. Accordingly, we carried out an open field test to analyse the effects of Pg-LPS. For comparison, effects of Ec-LPS were also studied. We additionally investigated the influence of systemic administration of Pg-LPS or Ec-LPS on IL-6, TNF-alpha, and IL-10 levels in blood, as they could be involved in the changes in locomotion. The TLR4 receptor antagonist TAK-242 was used to study the involvement of TLR4. Since Pg-LPS may block TLR4 in vitro, we analysed the effects of Pg-LPS on Ec-LPS-induced changes in behavioural and biochemical parameters. Male ddY mice were used. Pg- or Ec-LPS and TAK-242 were administered intraperitoneally. Ec-LPS (840 µg/kg), but not Pg-LPS (100, 500 and 840 µg/kg), inhibited novelty-induced locomotion, which was antagonized by TAK-242 (3.0 mg/kg). Ec-LPS (840 µg/kg) increased blood levels of IL-6 and IL-10, which were antagonized by TAK-242 (3.0 mg/kg). However, TAK-242 did not inhibit Ec-LPS-induced increases in TNF-alpha levels in blood. Pg-LPS (100, 500, and 840 µg/kg) did not alter blood IL-6, TNF-alpha, or IL-10 levels. The Ec-LPS-induced increase in blood IL-10, but not IL-6 and TNF-alpha, levels was inhibited by Pg-LPS (500 µg/kg). These results suggest that TLR4 stimulation mediates the inhibition of novel environment-induced locomotion in mice following systemic administration of Ec-LPS, while also increasing blood IL-6 and IL-10 levels. In contrast, Pg-LPS did not exhibit these effects. The present study also provides in vivo evidence that Pg-LPS can inhibit TLR4-mediated increases in blood levels of IL-10, a cytokine thought to prevent the development of periodontal disease.


Assuntos
Escherichia coli , Lipopolissacarídeos , Porphyromonas gingivalis , Receptor 4 Toll-Like , Animais , Receptor 4 Toll-Like/metabolismo , Camundongos , Masculino , Locomoção/efeitos dos fármacos , Citocinas/sangue , Citocinas/metabolismo , Interleucina-6/sangue , Interleucina-10/sangue , Fator de Necrose Tumoral alfa/sangue , Sulfonamidas
10.
Int Immunopharmacol ; 136: 112380, 2024 Jul 30.
Artigo em Inglês | MEDLINE | ID: mdl-38850790

RESUMO

BACKGROUND AND AIMS: Impaired intestinal barrier function is key in maintaining intestinal inflammation in Crohn's disease (CD). However, no targeted treatment in clinical practice has been developed. Peiminine (Pm) strongly protects the epithelial barrier, the purpose of this study is to investigate whether Pm affects CD-like colitis and potential mechanisms for its action. METHODS: Trinitro-benzene-sulfonic acid (TNBS)-induced mice and Il-10-/- mice were used as CD animal models. Colitis symptoms, histological analysis, and intestinal barrier permeability were used to assess the Pm's therapeutic effect on CD-like colitis. The colon organoids were induced by TNF-α to evaluate the direct role of Pm in inhibiting apoptosis of the intestinal epithelial cells. Western blotting and small molecule inhibitors were used to investigate further the potential mechanism of Pm in inhibiting apoptosis of intestinal epithelial cells. RESULTS: Pm treatment reduced body weight loss, disease activity index (DAI) score, and inflammatory score, demonstrating that colonic inflammation in mice were alleviated. Pm decreased the intestinal epithelial apoptosis, improved the intestinal barrier function, and prevented the loss of tight junction proteins (ZO1 and claudin-1) in the colon of CD mice and TNF-α-induced colonic organoids. Pm activated Nrf2/HO1 signaling, which may protect intestinal barrier function. CONCLUSIONS: Pm inhibits intestinal epithelial apoptosis in CD mice by activating Nrf2/HO1 pathway. This partially explains the potential mechanism of Pm in ameliorating intestinal barrier function in mice and provides a new approach to treating CD.


Assuntos
Apoptose , Colite , Doença de Crohn , Modelos Animais de Doenças , Mucosa Intestinal , Camundongos Endogâmicos C57BL , Camundongos Knockout , Fator 2 Relacionado a NF-E2 , Transdução de Sinais , Ácido Trinitrobenzenossulfônico , Animais , Fator 2 Relacionado a NF-E2/metabolismo , Doença de Crohn/tratamento farmacológico , Doença de Crohn/patologia , Mucosa Intestinal/efeitos dos fármacos , Mucosa Intestinal/patologia , Mucosa Intestinal/metabolismo , Colite/tratamento farmacológico , Colite/induzido quimicamente , Colite/patologia , Camundongos , Transdução de Sinais/efeitos dos fármacos , Apoptose/efeitos dos fármacos , Humanos , Masculino , Colo/patologia , Colo/efeitos dos fármacos , Heme Oxigenase-1/metabolismo , Heme Oxigenase-1/genética , Heme Oxigenase (Desciclizante)/metabolismo , Heme Oxigenase (Desciclizante)/genética , Interleucina-10/metabolismo , Anti-Inflamatórios/farmacologia , Anti-Inflamatórios/uso terapêutico , Proteínas de Membrana
11.
Cardiovasc Diabetol ; 23(1): 202, 2024 Jun 12.
Artigo em Inglês | MEDLINE | ID: mdl-38867293

RESUMO

The specific pathophysiological pathways through which diabetes exacerbates myocardial ischemia/reperfusion (I/R) injury remain unclear; however, dysregulation of immune and inflammatory cells, potentially driven by abnormalities in their number and function due to diabetes, may play a significant role. In the present investigation, we simulated myocardial I/R injury by inducing ischemia through ligation of the left anterior descending coronary artery in mice for 40 min, followed by reperfusion for 24 h. Previous studies have indicated that protein kinase Cß (PKCß) is upregulated under hyperglycemic conditions and is implicated in the development of various diabetic complications. The Y4 RNA fragment is identified as the predominant small RNA component present in the extracellular vesicles of cardio sphere-derived cells (CDCs), exhibiting notable anti-inflammatory properties in the contexts of myocardial infarction and cardiac hypertrophy. Our investigation revealed that the administration of Y4 RNA into the ventricular cavity of db/db mice following myocardial I/R injury markedly enhanced cardiac function. Furthermore, Y4 RNA was observed to facilitate M2 macrophage polarization and interleukin-10 secretion through the suppression of PKCß activation. The mechanism by which Y4 RNA affects PKCß by regulating macrophage activation within the inflammatory environment involves the inhibition of ERK1/2 phosphorylation In our study, the role of PKCß in regulating macrophage polarization during myocardial I/R injury was investigated through the use of PKCß knockout mice. Our findings indicate that PKCß plays a crucial role in modulating the inflammatory response associated with macrophage activation in db/db mice experiencing myocardial I/R, with a notable exacerbation of this response observed upon significant upregulation of PKCß expression. In vitro studies further elucidated the protective mechanism by which Y4 RNA modulates the PKCß/ERK1/2 signaling pathway to induce M2 macrophage activation. Overall, our findings suggest that Y4 RNA plays an anti-inflammatory role in diabetic I/R injury, suggesting a novel therapeutic approach for managing myocardial I/R injury in diabetic individuals.


Assuntos
Modelos Animais de Doenças , Macrófagos , Camundongos Endogâmicos C57BL , Traumatismo por Reperfusão Miocárdica , Proteína Quinase C beta , Transdução de Sinais , Animais , Proteína Quinase C beta/metabolismo , Traumatismo por Reperfusão Miocárdica/patologia , Traumatismo por Reperfusão Miocárdica/enzimologia , Traumatismo por Reperfusão Miocárdica/metabolismo , Traumatismo por Reperfusão Miocárdica/prevenção & controle , Traumatismo por Reperfusão Miocárdica/genética , Macrófagos/metabolismo , Macrófagos/enzimologia , Masculino , Interleucina-10/metabolismo , Interleucina-10/genética , Camundongos , Cardiomiopatias Diabéticas/enzimologia , Cardiomiopatias Diabéticas/patologia , Cardiomiopatias Diabéticas/metabolismo , Cardiomiopatias Diabéticas/etiologia , Cardiomiopatias Diabéticas/genética , Cardiomiopatias Diabéticas/fisiopatologia , Células Cultivadas , Fenótipo , Miócitos Cardíacos/enzimologia , Miócitos Cardíacos/patologia , Miócitos Cardíacos/metabolismo , Proteína Quinase 3 Ativada por Mitógeno/metabolismo , Ativação de Macrófagos , Proteína Quinase 1 Ativada por Mitógeno/metabolismo , Função Ventricular Esquerda , Fosforilação
12.
CNS Neurosci Ther ; 30(6): e14796, 2024 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-38867395

RESUMO

AIMS: The extent of perihematomal edema following intracerebral hemorrhage (ICH) significantly impacts patient prognosis, and disruption of the blood-brain barrier (BBB) exacerbates perihematomal edema. However, the role of peripheral IL-10 in mitigating BBB disruption through pathways that link peripheral and central nervous system signals remains poorly understood. METHODS: Recombinant IL-10 was administered to ICH model mice via caudal vein injection, an IL-10-inhibiting adeno-associated virus and an IL-10 receptor knockout plasmid were delivered intraventricularly, and neurobehavioral deficits, perihematomal edema, BBB disruption, and the expression of JAK1 and STAT3 were evaluated. RESULTS: Our study demonstrated that the peripheral cytokine IL-10 mitigated BBB breakdown, perihematomal edema, and neurobehavioral deficits after ICH and that IL-10 deficiency reversed these effects, likely through the IL-10R/JAK1/STAT3 signaling pathway. CONCLUSIONS: Peripheral IL-10 has the potential to reduce BBB damage and perihematomal edema following ICH and improve patient prognosis.


Assuntos
Edema Encefálico , Hemorragia Cerebral , Interleucina-10 , Janus Quinase 1 , Receptores de Interleucina-10 , Fator de Transcrição STAT3 , Transdução de Sinais , Animais , Fator de Transcrição STAT3/metabolismo , Hemorragia Cerebral/complicações , Hemorragia Cerebral/tratamento farmacológico , Hemorragia Cerebral/metabolismo , Edema Encefálico/etiologia , Edema Encefálico/tratamento farmacológico , Janus Quinase 1/metabolismo , Janus Quinase 1/antagonistas & inibidores , Interleucina-10/metabolismo , Transdução de Sinais/efeitos dos fármacos , Transdução de Sinais/fisiologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Barreira Hematoencefálica/efeitos dos fármacos , Barreira Hematoencefálica/metabolismo
13.
Actas Esp Psiquiatr ; 52(3): 317-324, 2024 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-38863039

RESUMO

BACKGROUND: Craniocerebral injuries can cause inflammation and oxidative stress, and can have permanent effects on cognitive function. Moreover, over time, excessive expression of inflammatory factors and high levels of oxidative stress will be detrimental to recovery from craniocerebral injury and may exacerbate neurological damage, further damaging neurons and other cellular structures. In this study, we investigated changes in inflammation and stress indicators in patients with severe craniocerebral injuries, and analyzed associations with concurrent cognitive impairment. METHODS: 82 patients with severe craniocerebral injuries admitted to Longyou County People's Hospital during January 2022-June 2023 were selected for retrospective study. Levels of inflammatory factors and the degree of oxidative stress were recorded and compared between the acute and chronic phases. Inflammatory measures included interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor-alpha (TNF-α) and C-reactive protein (CRP), and oxidative stress indicators included human cortisol (Cor), norepinephrine (NE), and superoxide dismutase (SOD). The patients' cognitive function was evaluated using the Mini-Mental State Examination (MMSE), and the incidence of cognitive impairment was assessed. Spearman's correlation was used to analyze associations between inflammatory and oxidative stress measures and MMSE scores; logistic regression was used to analyze the related factors affecting the patients' concurrent cognitive impairment; and the receiver operating characteristic (ROC) curve was used to test the predictive value of inflammatory and oxidative stress measures on the patients' concurrent cognitive impairment in the acute phase and the chronic phase. RESULTS: Patients had higher levels of IL-6, IL-10, TNF-α, CRP, Cor, and NE, and lower levels of SOD, in the acute phase compared to the chronic phase (p < 0.05). MMSE scores were higher in the acute phase than in the chronic phase (p < 0.05). A total of 50 cases were complicated by cognitive impairment, and the incidence of cognitive impairment was 60.98%. The levels of IL-6, IL-10, TNF-α, CRP, Cor, and NE in the chronic phase were positively correlated with the concurrent cognitive impairment, and the level of SOD was negatively correlated with the concurrent cognitive impairment (p < 0.05). Single-factor analysis showed that age and levels of IL-6, IL-10, TNF-α, CRP, Cor, and NE were higher in the cognitively impaired group than in the cognitively normal group, SOD levels were lower than in the cognitively normal group, and percentages of below-secondary school and frontal lobe damage were higher than those in the cognitively normal group (p < 0.05). Logistic regression analysis showed that below-secondary school, frontal lobe injury, higher levels of IL-6, IL-10, TNF-α, and CRP in the chronic phase, and lower levels of SOD in the chronic phase were all relevant factors affecting the patients' concurrent cognitive impairment. As shown by the ROC curve, the area under the curve (AUC) for the combination of indicators was 0.949, sensitivity was 0.980, and specificity was 0.844. CONCLUSIONS: The incidence of cognitive impairment is higher in patients with severe craniocerebral injury, and the levels of inflammation and oxidative stress, which are not conducive to recovery, are higher in patients in the acute stage. The risk of concurrent cognitive impairment is higher in patients with a lower level of literacy, frontal lobe injury, and high levels of inflammatory factors and oxidative stress in the chronic stage; these indicators, therefore, have a significant predictive effect on the prognosis of the patients.


Assuntos
Disfunção Cognitiva , Traumatismos Craniocerebrais , Inflamação , Estresse Oxidativo , Humanos , Disfunção Cognitiva/sangue , Disfunção Cognitiva/etiologia , Disfunção Cognitiva/epidemiologia , Feminino , Masculino , Inflamação/sangue , Pessoa de Meia-Idade , Estudos Retrospectivos , Adulto , Traumatismos Craniocerebrais/complicações , Traumatismos Craniocerebrais/sangue , Idoso , Interleucina-10/sangue , Proteína C-Reativa/metabolismo
14.
Nat Commun ; 15(1): 4309, 2024 Jun 03.
Artigo em Inglês | MEDLINE | ID: mdl-38830846

RESUMO

The efficacy of costimulation blockade with CTLA4-Ig (belatacept) in transplantation is limited due to T cell-mediated rejection, which also persists after induction with anti-thymocyte globulin (ATG). Here, we investigate why ATG fails to prevent costimulation blockade-resistant rejection and how this barrier can be overcome. ATG did not prevent graft rejection in a murine heart transplant model of CTLA4-Ig therapy and induced a pro-inflammatory cytokine environment. While ATG improved the balance between regulatory T cells (Treg) and effector T cells in the spleen, it had no such effect within cardiac allografts. Neutralizing IL-6 alleviated graft inflammation, increased intragraft Treg frequencies, and enhanced intragraft IL-10 and Th2-cytokine expression. IL-6 blockade together with ATG allowed CTLA4-Ig therapy to achieve long-term, rejection-free heart allograft survival. This beneficial effect was abolished upon Treg depletion. Combining ATG with IL-6 blockade prevents costimulation blockade-resistant rejection, thereby eliminating a major impediment to clinical use of costimulation blockers in transplantation.


Assuntos
Abatacepte , Soro Antilinfocitário , Rejeição de Enxerto , Sobrevivência de Enxerto , Transplante de Coração , Interleucina-6 , Linfócitos T Reguladores , Animais , Masculino , Camundongos , Abatacepte/farmacologia , Abatacepte/uso terapêutico , Aloenxertos/imunologia , Soro Antilinfocitário/farmacologia , Soro Antilinfocitário/uso terapêutico , Rejeição de Enxerto/imunologia , Rejeição de Enxerto/prevenção & controle , Sobrevivência de Enxerto/efeitos dos fármacos , Sobrevivência de Enxerto/imunologia , Transplante de Coração/efeitos adversos , Imunossupressores/farmacologia , Interleucina-10/metabolismo , Interleucina-10/imunologia , Interleucina-6/metabolismo , Depleção Linfocítica , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , Linfócitos T Reguladores/imunologia , Linfócitos T Reguladores/efeitos dos fármacos
15.
Gut Microbes ; 16(1): 2363020, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38841892

RESUMO

CD4+ T cells play a critical role in regulating autoimmune diseases, and intestinal microbial metabolites control various immune responses. Granzyme B (GzmB)-producing CD4+ T cells have been recently reported to participate in the pathogenesis of autoimmune diseases. Here, we found that GzmbB-deficient CD4+ T cells induced more severe colitis in Rag1-/- mice than wild-type (WT) CD4+ T cells. Germ-free (GF) mice exhibited a lower expression of GzmB in intestinal CD4+ T cells compared to specific pathogen-free (SPF) mice. Intestinal microbial metabolite butyrate increased GzmB expression in CD4+ T cells, especially in IL-10-producing Th1 cells, through HDAC inhibition and GPR43, but not GPR41 and GPR109a. Butyrate-treated GzmB-deficient CD4+ T cells demonstrated more severe colitis compared to butyrate-treated WT CD4+ T cells in the T cell transfer model. Butyrate altered intestinal microbiota composition, but altered microbiota did not mediate butyrate induction of intestinal CD4+ T cell expression of GzmB in mice. Blimp1 was involved in the butyrate induction of GzmB in IL-10-producing Th1 cells. Glucose metabolism, including glycolysis and pyruvate oxidation, mediated butyrate induction of GzmB in Th1 cells. In addition, we found that IKZF3 and NR2F6 regulated GzmB expression induced by butyrate. Together, our studies underscored the critical role of GzmB in mediating gut bacterial metabolite butyrate regulation of T cell tolerance at the mucosal surface.


Assuntos
Butiratos , Colite , Microbioma Gastrointestinal , Granzimas , Interleucina-10 , Camundongos Endogâmicos C57BL , Células Th1 , Animais , Interleucina-10/metabolismo , Interleucina-10/genética , Interleucina-10/imunologia , Células Th1/imunologia , Camundongos , Microbioma Gastrointestinal/efeitos dos fármacos , Butiratos/metabolismo , Butiratos/farmacologia , Granzimas/metabolismo , Colite/imunologia , Colite/microbiologia , Colite/metabolismo , Camundongos Knockout , Fator 1 de Ligação ao Domínio I Regulador Positivo/metabolismo , Fator 1 de Ligação ao Domínio I Regulador Positivo/genética , Receptores Acoplados a Proteínas G/metabolismo , Receptores Acoplados a Proteínas G/genética , Linfócitos T CD4-Positivos/imunologia , Linfócitos T CD4-Positivos/metabolismo , Tolerância Imunológica , Proteínas de Homeodomínio
16.
Front Immunol ; 15: 1373553, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38846955

RESUMO

Introduction: Staphylococcus aureus bacteremia (SAB) is a life-threatening infection particularly involving methicillin-resistant S. aureus (MRSA). In contrast to resolving MRSA bacteremia (RB), persistent MRSA bacteremia (PB) blood cultures remain positive despite appropriate antibiotic treatment. Host immune responses distinguishing PB vs. RB outcomes are poorly understood. Here, integrated transcriptomic, IL-10 cytokine levels, and genomic analyses sought to identify signatures differentiating PB vs. RB outcomes. Methods: Whole-blood transcriptomes of propensity-matched PB (n=28) versus RB (n=30) patients treated with vancomycin were compared in one independent training patient cohort. Gene expression (GE) modules were analyzed and prioritized relative to host IL-10 cytokine levels and DNA methyltransferase-3A (DNMT3A) genotype. Results: Differential expression of T and B lymphocyte gene expression early in MRSA bacteremia discriminated RB from PB outcomes. Significant increases in effector T and B cell signaling pathways correlated with RB, lower IL-10 cytokine levels and DNMT3A heterozygous A/C genotype. Importantly, a second PB and RB patient cohort analyzed in a masked manner demonstrated high predictive accuracy of differential signatures. Discussion: Collectively, the present findings indicate that human PB involves dysregulated immunity characterized by impaired T and B cell responses associated with excessive IL-10 expression in context of the DNMT3A A/A genotype. These findings reveal distinct immunologic programs in PB vs. RB outcomes, enable future studies to define mechanisms by which host and/or pathogen drive differential signatures and may accelerate prediction of PB outcomes. Such prognostic assessment of host risk could significantly enhance early anti-infective interventions to avert PB and improve patient outcomes.


Assuntos
Bacteriemia , Perfilação da Expressão Gênica , Staphylococcus aureus Resistente à Meticilina , Infecções Estafilocócicas , Transcriptoma , Humanos , Bacteriemia/diagnóstico , Bacteriemia/imunologia , Bacteriemia/genética , Bacteriemia/microbiologia , Infecções Estafilocócicas/imunologia , Infecções Estafilocócicas/genética , Infecções Estafilocócicas/diagnóstico , Infecções Estafilocócicas/microbiologia , Masculino , Feminino , Pessoa de Meia-Idade , Idoso , Interleucina-10/genética , Interleucina-10/sangue , DNA Metiltransferase 3A , Antibacterianos/uso terapêutico , Adulto
17.
Front Immunol ; 15: 1363457, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38855111

RESUMO

Introduction: Human infections with the food-borne enteropathogen Campylobacter jejuni are responsible for increasing incidences of acute campylobacteriosis cases worldwide. Since antibiotic treatment is usually not indicated and the severity of the enteritis directly correlates with the risk of developing serious autoimmune disease later-on, novel antibiotics-independent intervention strategies with non-toxic compounds to ameliorate and even prevent campylobacteriosis are utmost wanted. Given its known pleiotropic health-promoting properties, curcumin constitutes such a promising candidate molecule. In our actual preclinical placebo-controlled intervention trial, we tested the anti-microbial and anti-inflammatory effects of oral curcumin pretreatment during acute experimental campylobacteriosis. Methods: Therefore, secondary abiotic IL-10-/- mice were challenged with synthetic curcumin via the drinking water starting a week prior oral C. jejuni infection. To assess anti-pathogenic, clinical, immune-modulatory, and functional effects of curcumin prophylaxis, gastrointestinal C. jejuni bacteria were cultured, clinical signs and colonic histopathological changes quantitated, pro-inflammatory immune cell responses determined by in situ immunohistochemistry and intestinal, extra-intestinal and systemic pro-inflammatory mediator measurements, and finally, intestinal epithelial barrier function tested by electrophysiological resistance analysis of colonic ex vivo biopsies in the Ussing chamber. Results and discussion: Whereas placebo counterparts were suffering from severe enterocolitis characterized by wasting symptoms and bloody diarrhea on day 6 post-infection, curcumin pretreated mice, however, were clinically far less compromised and displayed less severe microscopic inflammatory sequelae such as histopathological changes and epithelial cell apoptosis in the colon. In addition, curcumin pretreatment could mitigate pro-inflammatory innate and adaptive immune responses in the intestinal tract and importantly, rescue colonic epithelial barrier integrity upon C. jejuni infection. Remarkably, the disease-mitigating effects of exogenous curcumin was also observed in organs beyond the infected intestines and strikingly, even systemically given basal hepatic, renal, and serum concentrations of pro-inflammatory mediators measured in curcumin pretreated mice on day 6 post-infection. In conclusion, the anti-Campylobacter and disease-mitigating including anti-inflammatory effects upon oral curcumin application observed here highlight the polyphenolic compound as a promising antibiotics-independent option for the prevention from severe acute campylobacteriosis and its potential post-infectious complications.


Assuntos
Infecções por Campylobacter , Campylobacter jejuni , Curcumina , Animais , Curcumina/administração & dosagem , Curcumina/farmacologia , Infecções por Campylobacter/tratamento farmacológico , Infecções por Campylobacter/imunologia , Camundongos , Campylobacter jejuni/efeitos dos fármacos , Administração Oral , Camundongos Knockout , Modelos Animais de Doenças , Camundongos Endogâmicos C57BL , Interleucina-10/metabolismo , Doença Aguda , Antibacterianos/administração & dosagem
18.
Int Heart J ; 65(3): 498-505, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38825494

RESUMO

This study aimed to explore the expression of long non-coding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (NEAT1) in patients with acute myocardial infarction (AMI) and its inflammatory regulation mechanism through miR-211/interleukin 10 (IL-10) axis.A total of 75 participants were enrolled in this study: 25 healthy people in the control group, 25 patients with stable angina pectoris (SAP) in the SAP group, and 25 patients with AMI in the AMI group. Real-time qPCR was used to detect mRNA expression levels of NEAT1, miR-211, and IL-10. The interaction between miR-211, NEAT1, and IL-10 was confirmed by dual-luciferase reporter assay, and protein expression was detected using western blot.High expression of NEAT1 in peripheral blood mononuclear cells (PBMCs) of patients with AMI was negatively related to serum creatine kinase-MB (CK-MB), cardiac troponin I (cTnI), tumor necrosis factor-α (TNF-α), IL-6, and IL-1ß and was positively correlated with left ventricular ejection fraction (LVEF). In THP-1 cells, miR-211 was confirmed to target and inhibit IL-10 expression. NEAT1 knockdown and miR-211-mimic markedly decreased IL-10 protein levels, whereas anti-miR-211 markedly increased IL-10 protein levels. Importantly, miR-211 level was negatively related to NEAT1 and IL-10 levels, whereas IL-10 level was positively related to the level of NEAT1 expression in PBMCs of patients with AMI.LncRNA NEAT1 was highly expressed in PBMCs of patients with AMI, and NEAT1 suppressed inflammation via miR-211/IL-10 axis in PBMCs of patients with AMI.


Assuntos
Interleucina-10 , Leucócitos Mononucleares , MicroRNAs , Infarto do Miocárdio , RNA Longo não Codificante , Humanos , RNA Longo não Codificante/genética , RNA Longo não Codificante/sangue , MicroRNAs/sangue , MicroRNAs/genética , Interleucina-10/sangue , Interleucina-10/metabolismo , Infarto do Miocárdio/sangue , Infarto do Miocárdio/genética , Infarto do Miocárdio/metabolismo , Leucócitos Mononucleares/metabolismo , Masculino , Feminino , Pessoa de Meia-Idade , Idoso , Inflamação/genética , Inflamação/sangue , Inflamação/metabolismo , Estudos de Casos e Controles
19.
Trop Biomed ; 41(1): 70-77, 2024 Mar 01.
Artigo em Inglês | MEDLINE | ID: mdl-38852136

RESUMO

The study aimed to compare and correlate serum levels of IL-6, 10, and 25-hydroxycholecalciferol in individuals with asthma with and without post-COVID condition (PCC). The study was designed to investigate the inflammatory response and serum 25-hydroxycholecalciferol status in asthmatics with and without PCC. A cross-sectional study of 252 subjects (128 asthmatics and 124 non-asthmatic subjects) was carried out. Interleukins and 25-hydroxycholecalciferol levels were estimated on ELISA. The principle findings were that IL-6 and 25-hydroxycholecalciferol levels were significantly increased (p<0.001), while IL-10 levels were non-significant in asthmatics with PCC compared to those without PCC. However, 25-hydroxycholecalciferol levels were significantly increased, but no significant change was observed in IL-6, and IL-10 levels in non-asthmatics with and without chronic PCC. A significant positive correlation (r = 0.258) was found between 25-hydroxycholecalciferol and IL-6 but a significant negative correlation (r = -0.227) with IL-10 in asthmatics with PCC. Similarly, a significant negative correlation (r = -0.285) was found between 25-hydroxycholecalciferol and IL-10 but was non-significant with IL-6 in asthmatics without PCC. The correlation of 25-hydroxycholecalciferol with IL-10 was significant (0.683), but IL-6 was non-significant in non-asthmatics with PCC. Multiple regression analysis showed that age, IL-6, gender, and PCC were significantly related in adjusted values to 25-hydroxycholecalciferol. This study sheds light on the complex liaison between 25-hydroxycholecalciferol levels and inflammatory responses in asthmatics, especially those with PCC. The findings suggest that although asthmatics with PCC maintain sufficient levels of 25-hydroxycholecalciferol, they show a substantial increase in the proinflammatory response. This suggests that PCC exacerbates the pro-inflammatory response in asthma. Moreover, the study reveals that asthmatics, whether with or without PCC, display a negative correlation between 25-hydroxycholecalciferol and the anti-inflammatory response. This emphasizes the main influence of asthma on the overall inflammatory response. These findings reveal a complex interplay between vitamin D levels and inflammatory mediators in asthmatic individuals with and without PCC.


Assuntos
Asma , COVID-19 , Calcifediol , Interleucina-10 , Interleucina-6 , Humanos , Masculino , Feminino , Estudos Transversais , Adulto , Interleucina-6/sangue , Interleucina-10/sangue , Calcifediol/sangue , Pessoa de Meia-Idade , COVID-19/sangue , COVID-19/complicações , SARS-CoV-2 , Doença Crônica
20.
Exp Gerontol ; 193: 112480, 2024 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-38852656

RESUMO

BACKGROUND: The role of interleukins in sarcopenia development has been acknowledged, yet the specifics of their involvement remain to be fully understood. This study aimed to explore alterations in interleukin levels among sarcopenia patients. METHODS: Searches were conducted in Embase, Medline, and the Cochrane Library for literature published up to May 2023. Eligible observational studies with a diagnosis of sarcopenia were included. The Newcastle-Ottawa Scale was utilized for quality assessment. For data synthesis, a random-effects model was used, and the Mantel-Haenszel method was used for pooled estimates. RESULTS: Of the 7685 articles screened, 37 met the inclusion criteria. Statistically significant differences in the levels of IL-1ß, IL-6 and IL-10 were detected in sarcopenia patients. Specifically, IL-1ß (95 % CI: 0.33 [0.12, 0.54], P < 0.05), IL-6 (95 % CI: 0.91 [0.59, 1.24], P < 0.05), and IL-10 (95 % CI: 0.11 [0.07,0.15], P < 0.05) were detected. However, no significant associations were found between serum IL-4 (95 % CI: 0.36 [-0.18, 0.42], P = 0.44), IL-8 (95 % CI: -1.05 [-3.06, 0.95], P = 0.3), IL-12 (95 % CI: -3.92 [-8.32,0.48], P = 0.08) or IL-17 (95 % CI: 0.22 [-2.43, 2.88], P = 0.87) and sarcopenia. Subgroup analysis showed no significant difference in IL-6 (95 % CI: -0.03 [-0.72, 0.66], P = 0.93) and IL-10 (95 % CI: 0.1 [-0.44, 0.64], P = 0.72) among patients with European standard sarcopenia. CONCLUSIONS: Inflammation plays a role in sarcopenia, and the serum levels of IL-1ß, IL-6, and IL-10 are associated with sarcopenia. Further research is needed to clarify these associations. CLINICAL TRIALS REGISTRATION NUMBER: CRD42024506656.


Assuntos
Interleucinas , Sarcopenia , Idoso , Humanos , Interleucina-10/sangue , Interleucina-1beta/sangue , Interleucina-6/sangue , Interleucinas/sangue , Sarcopenia/sangue
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