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1.
J Agric Food Chem ; 69(25): 7016-7027, 2021 Jun 30.
Artigo em Inglês | MEDLINE | ID: mdl-34060828

RESUMO

Daily intake of tea has been known to relate to a low risk of depression. In this study, we report that a special variety of tea in China, Camellia assamica var. kucha (kucha), possesses antidepressant effects but with less adverse effects as compared to traditional tea Camellia sinensis. This action of kucha is related to its high amount of theacrine, a purine alkaloid structurally similar to caffeine. We investigated the antidepressant-like effects and mechanisms of theacrine in chronic water immersion restraint stress and chronic unpredictable mild stress mice models. PC12 cells and primary hippocampal neural stem cells were treated with stress hormone corticosterone (CORT) to reveal the potential antidepression mechanism of theacrine from the perspective of adult hippocampus neurogenesis. Results of behavioral and neurotransmitter analysis showed that intragastric administration of theacrine significantly counteracted chronic stress-induced depression-like disorders and abnormal 5-hydroxytryptamine (5-HT) metabolism with less central excitability. Further investigation from both in vivo and in vitro experiments indicated that the antidepressant mechanism of theacrine was associated with promoting adult hippocampal neurogenesis, via the modulation of the phosphodiesterase-4 (PDE4)/cyclic adenosine monophosphate (cAMP)/cAMP response-element binding (CREB)/brain-derived neurotrophic factor (BDNF)/tropomyosin-related kinase B (TrkB) pathway. Collectively, our findings could promote the prevalence of kucha as a common beverage with uses for health care and contribute to the development of theacrine as a potential novel antidepressant medicine.


Assuntos
Alcaloides , Camellia sinensis , Animais , Antidepressivos , Fator Neurotrófico Derivado do Encéfalo/genética , China , Depressão/tratamento farmacológico , Hipocampo , Camundongos , Neurogênese , Purinas , Ratos , Estresse Psicológico , Chá , Ácido Úrico/análogos & derivados
2.
Zhongguo Zhong Yao Za Zhi ; 46(4): 944-950, 2021 Feb.
Artigo em Chinês | MEDLINE | ID: mdl-33645101

RESUMO

Two new sucrose cinnamates(1 and 2) along with nine known compounds(3-11) were isolated from ethanol extract of Polygonum lapathifolium var. salicifolium by silica gel column chromatography, ODS column chromatography and semi-preparative HPLC. Their structures were elucidated by extensive spectroscopic methods including 1 D-and 2 D-NMR experiments, as well as HR-ESI-MS analysis. Eleven compounds(7 sucrose cinnamates, 3 phenylpropanoids and 1 lactone) were obtained and their structures were identified as(1,3-O-di-p-coumaroyl)-ß-D-fructofuranosyl-(2→1)-α-D-glucopyranoside(1),(1,3-O-di-p-coumaroyl)-ß-D-fructofuranosyl-(2→1)-(6-O-acetyl)-α-D-glucopyranoside(2),(3-O-feruloyl)-ß-D-fructofuranosyl-(2→1)-(6-O-p-coumaroyl)-α-D-glucopyranoside(3), hydropiperoside(4), vanicoside C(5),(1,3-O-di-p-coumaroyl)-ß-D-fructofuranosyl-(2→1)-(6-O-feruloyl)-α-D-glucopyranoside(6), vanicoside B(7),trans-p-hydroxycinnamic acid methyl ester(8), trans-p-hydroxycinnamic acid ethyl ester(9), methyl ferulate(10) and dimethoxydimethylphthalide(11), respectively. Compounds 1 and 2 were two new sucrose cinnamates, and compounds 1-11 were isolated from this plant for the first time. The antioxidant activities of the isolated compounds 1-9 were investigated by an oxygen radical absorbance capacity(ORAC) assay, and all nine compounds were found to show strong antioxidant activities. Among them, compound 6(10 µmol·L~(-1)) was the supreme one in antioxidant activities, with its ORAC value equivalent to(1.60±0.05) times of 50 µmol·L~(-1) Trolox.


Assuntos
Polygonum , Antioxidantes , Cinamatos , Ésteres , Estrutura Molecular , Sacarose
3.
FASEB J ; 34(8): 10998-11014, 2020 08.
Artigo em Inglês | MEDLINE | ID: mdl-32619083

RESUMO

Chronic stress-evoked depression has been implied to associate with the decline of adult hippocampal neurogenesis. Caffeine has been known to combat stress-evoked depression. Herein, we aim to investigate whether the protective effect of caffeine on depression is related with improving adult hippocampus neurogenesis and explore the mechanisms. Mouse chronic water immersion restraint stress (CWIRS) model, corticosterone (CORT)-established cell stress model, a coculture system containing CORT-treated BV-2 cells and hippocampal neural stem cells (NSCs) were utilized. Results showed that CWIRS caused obvious depressive-like disorders, abnormal 5-HT signaling, and elevated-plasma CORT levels. Notably, microglia activation-evoked brain inflammation and inhibited neurogenesis were also observed in the hippocampus of stressed mice. In comparison, intragastric administration of caffeine (10 and 20 mg/kg, 28 days) significantly reverted CWIRS-induced depressive behaviors, neurogenesis recession and microglia activation in the hippocampus. Further evidences from both in vivo and in vitro mechanistic experiments demonstrated that caffeine treatment significantly suppressed microglia activation via the A2AR/MEK/ERK/NF-κB signaling pathway. The results suggested that CORT-induced microglia activation contributes to stress-mediated neurogenesis recession. The antidepression effect of caffeine was associated with unlocking microglia activation-induced neurogenesis inhibition.


Assuntos
Cafeína/farmacologia , Corticosterona/farmacologia , Hipocampo/efeitos dos fármacos , Microglia/efeitos dos fármacos , Neurogênese/efeitos dos fármacos , Estresse Fisiológico/efeitos dos fármacos , Animais , Antidepressivos/farmacologia , Depressão/tratamento farmacológico , Depressão/metabolismo , Modelos Animais de Doenças , Hipocampo/metabolismo , Masculino , Camundongos , Microglia/metabolismo , Células-Tronco Neurais/efeitos dos fármacos , Células-Tronco Neurais/metabolismo , Serotonina/metabolismo , Transdução de Sinais/efeitos dos fármacos
4.
Theranostics ; 8(20): 5713-5730, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30555576

RESUMO

Skin cells are vulnerable to oxidative stress-induced senescence, which may lead to abnormal aging or aging-related disorders. Therefore, strategies that can ameliorate oxidative stress-induced senescence are expected to protect skin from damage, holding the promise of treating skin diseases in the clinic. This study aims to investigate whether caffeine, a well-known purine alkaloid, is able to prevent skin from oxidative stress-induced senescence, and to explore the underlying molecular mechanisms. Methods: A free radical inducer 2,2'-Azobis (2-amidinopropane) dihydrochloride (AAPH) was used to induce oxidative stress and cellular senescence in both transformed skin cells and in normal human epidermal keratinocytes (NHEKs). Ultraviolet (UV) irradiation was established as the in vivo oxidative stress model in mouse skin tissues. Cellular senescence was determined by SA ß-galactosidase staining, immunofluorescence and western blotting. Activation of autophagy was confirmed by western blotting, immunofluorescence, and transmission electron microscopy. Reactive oxygen species (ROS) detection by commercial kits, gene knockdown by RNA interference (RNAi) and receptor activation/inactivation by agonist/antagonist treatment were applied in mechanistic experiments. Results: We report that AAPH induced senescence in both transformed skin cells and in NHEKs. Similarly, UV irradiation induced senescence in mouse skin tissues. Remarkably, low dose of caffeine (<10 µM) suppressed cellular senescence and skin damage induced by AAPH or UV. Mechanistically, caffeine facilitated the elimination of ROS by activating autophagy. Using a combination of RNAi and chemical treatment, we demonstrate that caffeine activates autophagy through a series of sequential events, starting from the inhibition of its primary cellular target adenosine A2a receptor (A2AR) to an increase in the protein level of Sirtuin 3 (SIRT3) and to the activation of 5' adenosine monophosphate-activated protein kinase (AMPK). Oral administration of caffeine increased the protein level of SIRT3, induced autophagy, and reduced senescence and tissue damage in UV-irradiated mouse skin. On the other hand, co-administration with autophagy inhibitors attenuated the protective effect of caffeine on UV-induced skin damage in mice. Conclusion: The results reveal that caffeine protects skin from oxidative stress-induced senescence through activating the A2AR/SIRT3/AMPK-mediated autophagy. Our study not only demonstrated the beneficial effect of caffeine using both in vitro and in vivo models, but also systematically investigated the underlying molecular mechanisms. These discoveries implicate the potential of caffeine in the protection of skin disease.


Assuntos
Autofagia/efeitos dos fármacos , Cafeína/administração & dosagem , Oxidantes/toxicidade , Estresse Oxidativo , Dermatopatias/prevenção & controle , Raios Ultravioleta , Envelhecimento/patologia , Amidinas/toxicidade , Animais , Antioxidantes/administração & dosagem , Células Cultivadas , Modelos Animais de Doenças , Humanos , Camundongos , Modelos Teóricos , Pele/efeitos dos fármacos , Pele/efeitos da radiação , Dermatopatias/patologia , Resultado do Tratamento
5.
Metabolism ; 85: 227-239, 2018 08.
Artigo em Inglês | MEDLINE | ID: mdl-29727630

RESUMO

OBJECTIVE: Acylcarnitine metabolism disorder contributes significantly to the pathogenesis of nonalcoholic fatty liver disease (NAFLD). There are, however, few ideal medications for NAFLD, which work by targeting acylcarnitine metabolism. The aim of this study was to investigate the protective effects of theacrine, a rare purine alkaloid isolated from Camellia assamica var. kucha, against acylcarnitine metabolism disorder in NAFLD. METHODS: The pharmacological activities of theacrine were studied using high-fat diet (HFD)-fed ApoE-/- and C57BL/6J mice models. Oleate-treated HepG2 and L-02 cells were used to investigate the molecular mechanism of theacrine on acylcarnitine metabolism. The target of theacrine was confirmed in vitro as the blockade of sirtuin 3 (SIRT3) and protein kinase A. RESULTS: Theacrine inhibits hepatic steatosis and liver inflammation and improves energy expenditure in HFD-fed mice. Theacrine ameliorates acylcarnitine metabolism disorder in HFD-fed mice and oleate-treated hepatocytes by improving fatty acid oxidation. The underlying mechanism involves theacrine's activation of the mitochondrial deacetylase SIRT3 and consequently, the increased activity of long-chain acyl coenzyme A dehydrogenase (LCAD) through deacetylation. CONCLUSION: Theacrine promotes acylcarnitine metabolism in NAFLD through the SIRT3/LCAD signaling pathway. The target of theacrine's activities on NAFLD is identified as SIRT3.


Assuntos
Carnitina/análogos & derivados , Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico , Extratos Vegetais/uso terapêutico , Substâncias Protetoras/uso terapêutico , Ácido Úrico/análogos & derivados , Animais , Apolipoproteínas E/genética , Apolipoproteínas E/metabolismo , Carnitina/metabolismo , Dieta Hiperlipídica/efeitos adversos , Metabolismo Energético/efeitos dos fármacos , Masculino , Camundongos , Camundongos Knockout , Hepatopatia Gordurosa não Alcoólica/etiologia , Hepatopatia Gordurosa não Alcoólica/metabolismo , Ácido Oleico , Extratos Vegetais/farmacologia , Substâncias Protetoras/farmacologia , Transdução de Sinais/efeitos dos fármacos , Ácido Úrico/farmacologia , Ácido Úrico/uso terapêutico
6.
Redox Biol ; 14: 1-6, 2018 04.
Artigo em Inglês | MEDLINE | ID: mdl-28826042

RESUMO

Oxidative DNA damage in bone marrow cells is the main side effect of chemotherapy drugs including cyclophosphamide (CTX). However, not all antioxidants are effective in inhibiting oxidative DNA damage. In this study, we report the beneficial effect of carnosine (ß-alanyl-l-histidine), a special antioxidant with acrolein-sequestering ability, on CTX-induced bone marrow cell suppression. Our results show that carnosine treatment (100 and 200mg/kg, i.p.) significantly inhibited the generation of reactive oxygen species (ROS) and 8-hydroxy-2'-deoxyguanosine (8-oxo-dG), and decreased chromosomal abnormalities in the bone marrow cells of mice treated with CTX (20mg/kg, i.v., 24h). Furthermore, carnosine evidently mitigated CTX-induced G2/M arrest in murine bone marrow cells, accompanied by reduced ratios of p-Chk1/Chk1 and p-p53/p53 as well as decreased p21 expression. In addition, cell apoptosis caused by CTX was also suppressed by carnosine treatment, as assessed by decreased TUNEL-positive cell counts, down-regulated expressions of Bax and Cyt c, and reduced ratios of cleaved Caspase-3/Caspase-3. These results together suggest that carnosine can protect murine bone marrow cells from CTX-induced DNA damage via its antioxidant activity.


Assuntos
Antioxidantes/farmacologia , Carnosina/farmacologia , Ciclofosfamida/toxicidade , Dano ao DNA/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , 8-Hidroxi-2'-Desoxiguanosina , Animais , Antioxidantes/química , Células da Medula Óssea/citologia , Células da Medula Óssea/efeitos dos fármacos , Células da Medula Óssea/metabolismo , Carnosina/química , Caspase 3/metabolismo , Pontos de Checagem do Ciclo Celular/efeitos dos fármacos , Células Cultivadas , Quinase 1 do Ponto de Checagem/metabolismo , Aberrações Cromossômicas/efeitos dos fármacos , Inibidor de Quinase Dependente de Ciclina p21/metabolismo , Desoxiguanosina/análogos & derivados , Desoxiguanosina/química , Desoxiguanosina/metabolismo , Masculino , Camundongos , Microscopia Confocal , Espécies Reativas de Oxigênio/metabolismo , Proteína Supressora de Tumor p53/metabolismo
7.
Exp Biol Med (Maywood) ; 243(1): 66-77, 2018 01.
Artigo em Inglês | MEDLINE | ID: mdl-29078731

RESUMO

Polypeptides extracted from animal immune organs have been proved to exert immunomodulatory activities in previous reports. However, relative experimental data regarding the influence of a polypeptide mixture extracted from healthy calf spleen (lienal polypeptide [LP]) on the immune function in tumor therapy are limited, and the components in LP remain unclear. In the present study, the immune regulatory effect of LP was investigated in normal mice and Lewis lung carcinoma (LLC)-bearing mice treated with cyclophosphamide (CTX). The components of LP were identified by liquid chromatography-electrospray ionization-coupled with tandem mass spectrometry (LC-MS/MS) analysis and bioinformatic analysis. In LLC-bearing mice, LP showed a synergic antitumor effect with CTX, whereas LP alone did not present direct antitumor activity. Further, LP was found to enhance immune organ indexes, splenocyte number, and T lymphocyte subsets in normal mice and LLC-bearing mice treated with CTX. The decline of white blood cell and platelet counts, splenocyte proliferation activity, and peritoneal macrophage phagocytic function caused by CTX were also significantly suppressed by LP treatment in LLC-bearing mice. Notably, LP treatment significantly decreased the expression of phagocytosis-related proteins including CD47/signal regulatory protein α/Src homology phosphatase-1 in the tumor tissue of LLC-bearing mice treated with CTX. LC-MS/MS-based peptidomics unraveled the main polypeptides in LP with a length from 8 to 25 amino acids. Bioinformatics analysis further confirmed the possibility of LP to regulate immunity, especially in phagocytosis-related pathway. Our above findings indicated that LP can relieve the immunosuppression induced by chemotherapy and is a beneficial supplement in cancer therapy. Impact statement The immunomodulatory activities of polypeptides extracted from animal immune organs have incurred people's interests since a long time ago. In this study, we investigated the immune regulation effects of a polypeptide mixture extracted from health calf spleen (lienal polypeptide [LP]) in Lewis lung carcinoma-bearing mice treated with cyclophosphamide (CTX). Liquid chromatography-electrospray ionization-coupled with tandem mass spectrometry-based peptidomics and bioinformatics analysis unraveled the main polypeptides in LP and further confirmed that LP is mainly associated with immune regulating pathway, especially in tumor cell phagocytosis-related pathway. Our study for the first time revealed that polypeptides from spleen can relieve the immunosuppression induced by CTX and is a beneficial supplement in cancer therapy.


Assuntos
Antineoplásicos/administração & dosagem , Carcinoma Pulmonar de Lewis/tratamento farmacológico , Carcinoma Pulmonar de Lewis/imunologia , Fatores Imunológicos/administração & dosagem , Imunossupressores/administração & dosagem , Peptídeos/administração & dosagem , Baço/química , Animais , Bovinos , Cromatografia Líquida , Modelos Animais de Doenças , Masculino , Camundongos Endogâmicos C57BL , Peptídeos/isolamento & purificação , Espectrometria de Massas em Tandem , Resultado do Tratamento
8.
Nat Prod Res ; 30(12): 1404-10, 2016 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-26222269

RESUMO

Marsilea quadrifolia is an edible aquatic medicinal plant used as a traditional health food in Asia. Four new polyphenols including kaempferol 3-O-(2″-O-E-caffeoyl)-ß-d-glucopyranoside (1), kaempferol 3-O-(3″-O-E-caffeoyl)-α-l-arabinopyranoside (3), 4-methy-3'-hydroxypsilotinin (4) and (±)-(E)-4b-methoxy-3b,5b-dihydroxyscirpusin A (18) together with 14 known ones (2, 5-17) were isolated from the ethanol extract of M. quadrifolia. Structures of the new compounds were elucidated by extensive spectroscopic analyses. In DPPH and oxygen radical absorbance capacity antioxidant assays, some compounds showed stronger antioxidant activities and quercetin (9) was the most potent antioxidant in both assays. In a restraint-induced oxidative stress model in mice, quercetin significantly attenuated the increase in plasma ALT and AST levels as well as liver MDA content of restrained mice. Liver SOD activity was also significantly increased by quercetin, indicating a significant in vivo antioxidant activity. As a rich source of polyphenols with strong antioxidant activities, M. quadrifolia may be developed to a product for relieving oxidative stress.


Assuntos
Antioxidantes/farmacologia , Marsileaceae/química , Polifenóis/isolamento & purificação , Polifenóis/farmacologia , Animais , Antioxidantes/química , Ásia , Avaliação Pré-Clínica de Medicamentos/métodos , Etanol/química , Concentração Inibidora 50 , Fígado/efeitos dos fármacos , Fígado/metabolismo , Masculino , Malondialdeído/metabolismo , Camundongos , Estrutura Molecular , Estresse Oxidativo/efeitos dos fármacos , Extratos Vegetais/química , Plantas Medicinais/química , Polifenóis/química , Quercetina/farmacologia
9.
Food Funct ; 6(8): 2578-87, 2015 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-26114447

RESUMO

The beneficial effect of caffeine-containing food on non-alcoholic fatty liver disease (NAFLD) has been widely reported. The aim of this study was to explore the effect of caffeine on hepatic steatosis. C57BL/6 mice were randomly assigned to a normal diet or a high energy diet (HED). Caffeine was given to HED mice by oral gavage. Body weights, lipids in the liver and liver damage were measured. Meanwhile, cAMP, SIRT3 or AMPK inhibitors were treated respectively before incubation with caffeine in oleate-treated HepG2 cells. SIRT3 was further silenced by siRNA to confirm the results. Caffeine significantly decreased the mass of fat tissues, lipids, ALT and AST levels in the liver of HED-treated mice. Caffeine increased the transformation of ADP to ATP and activated the cAMP/CREB/SIRT3/AMPK/ACC pathway in the liver. Nile red staining demonstrated that suppression of cAMP, SIRT3 or AMPK in oleate-treated HepG2 cells counteracted the effect of caffeine. Moreover, knocking down SIRT3 could down-regulate AMPK and ACC phosphorylation by caffeine. These results demonstrate that caffeine could improve HED-induced hepatic steatosis by promoting lipid metabolism via the cAMP/CREB/SIRT3/AMPK/ACC pathway. SIRT3 functioned as a molecular bridge connecting caffeine and lipid metabolism.


Assuntos
Cafeína/administração & dosagem , Metabolismo dos Lipídeos , Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico , Sirtuína 3/metabolismo , Proteínas Quinases Ativadas por AMP/genética , Proteínas Quinases Ativadas por AMP/metabolismo , Acetil-CoA Carboxilase/genética , Acetil-CoA Carboxilase/metabolismo , Animais , Proteína de Ligação a CREB/genética , Proteína de Ligação a CREB/metabolismo , Dieta Hiperlipídica/efeitos adversos , Humanos , Fígado/efeitos dos fármacos , Fígado/enzimologia , Fígado/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Hepatopatia Gordurosa não Alcoólica/enzimologia , Hepatopatia Gordurosa não Alcoólica/genética , Hepatopatia Gordurosa não Alcoólica/metabolismo , Sirtuína 3/genética
10.
Int J Food Sci Nutr ; 65(7): 874-80, 2014 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-24932810

RESUMO

Long-term stress exposure can lead to disturbed homeostasis and cause many life-style diseases. Phloridzin possesses various bioactivities, but the understanding of the effects of phloridzin on stress-related lipid metabolism disorder is limited. Our results demonstrate that phloridzin improved plasma lipoprotein lipase (LPL) activity and triglyceride metabolism in restrained mice. A decrease of angiopoietin-like protein 4 (ANGPTL4) mRNA expression and an increase of AMP-activated protein kinase (AMPK) phosphorylation were observed after phloridzin treatment. After inhibiting AMPK phosphorylation, the effects of phloridzin on the amelioration of plasma LPL activity and suppression of ANGPTL4 expression were blocked. In addition, cardiac AMPK phosphorylation, plasma LPL activity and ANGPTL4 expression were also affected by phloridzin, even if the glucocorticoid receptor was blocked. Taken together, the down-regulation of ANGPTL4 expression by phloridzin was probably via a direct activation of AMPK pathway. This discovery can provide a biochemical and nutritional basis for the use of phloridzin-containing food and beverage in daily life.


Assuntos
Proteínas Quinases Ativadas por AMP/metabolismo , Angiopoietinas/metabolismo , Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos , Lipase Lipoproteica/metabolismo , Florizina/farmacologia , Estresse Fisiológico , Angiopoietinas/genética , Animais , Masculino , Camundongos , Mifepristona , Estresse Oxidativo , Fosforilação , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Receptores de Glucocorticoides/genética , Receptores de Glucocorticoides/metabolismo , Restrição Física , Triglicerídeos/sangue , Regulação para Cima
11.
Int J Food Sci Nutr ; 65(5): 594-601, 2014 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-24548119

RESUMO

Bilberry (Vaccinium myrtillus L.) has been known to play a protective role in human health due to its high anthocyanin content. This study investigated the anti-inflammatory effects of bilberry extract (BE, containing 42.04% anthocyanin) on Propionibacterium acnes (P. acnes) plus lipopolysaccharide (LPS) induced liver injury and croton oil-induced ear edema in mice. Results showed that BE could effectively inhibit croton oil-induced ear edema and liver inflammation provoked by P. acnes plus LPS, as reflected by the reduced plasma alanine aminotransferase and aspartate aminotransferase activities. These findings were confirmed by hepatic pathological examination. Moreover, BE administration markedly suppressed the increase of liver mRNA levels of iNOS, TNF-α, IL-1ß and IL-6, and the protein levels of iNOS, TNF-α and NF-κB. In addition, liver malondialdehyde and NO contents were significantly reduced by BE treatment. These results indicated that BE has potent protective effects on acute and immunological inflammation, which might contribute to the study of the anti-inflammatory effects of natural products and healthy food.


Assuntos
Antocianinas/farmacologia , Anti-Inflamatórios/farmacologia , Doença Hepática Induzida por Substâncias e Drogas/tratamento farmacológico , Edema/tratamento farmacológico , Propionibacterium acnes/efeitos dos fármacos , Alanina Transaminase/sangue , Animais , Aspartato Aminotransferases/sangue , Óleo de Cróton/efeitos adversos , Edema/induzido quimicamente , Interleucina-1beta/genética , Interleucina-1beta/metabolismo , Interleucina-6/genética , Interleucina-6/metabolismo , Lipopolissacarídeos/efeitos adversos , Fígado/efeitos dos fármacos , Fígado/metabolismo , Masculino , Malondialdeído/metabolismo , Camundongos , NF-kappa B/genética , NF-kappa B/metabolismo , Óxido Nítrico/metabolismo , Óxido Nítrico Sintase Tipo II/genética , Óxido Nítrico Sintase Tipo II/metabolismo , Extratos Vegetais , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/metabolismo , Vaccinium myrtillus/química
12.
World J Emerg Med ; 1(3): 209-11, 2010.
Artigo em Inglês | MEDLINE | ID: mdl-25214970

RESUMO

BACKGROUND: Acute kidney injury (AKI) is associated with a high mortality. This study was undertaken to detect the factors associated with the prognosis of AKI. METHODS: We retrospectively reviewed 98 patients with AKI treated from March 2008 to August 2009 at this hospital. In these patients, 60 were male and 38 female. Their age ranged from 19 to 89 years (mean 52.4±16.1 years). The excluded patients were those who died within 24 hours after admission to ICU or those who had a history of chronic kidney disease or incomplete data. After 60 days of treatment, the patients were divided into a survival group and a death group. Clinical data including gender, age, history of chronic diseases, the worst laboratory values within 24 hours after diagnosis (values of routine blood tests, blood gas analysis, liver and renal function, levels of serum cystatin C, and blood electrolytes) were analyzed. Acute physiology, chronic health evaluation (APACHE) II scores and 60-day mortality were calculated. Univariate analysis was performed to find variables relevant to prognosis, odds ratio (OR) and 95% confidence interval (CI). Multiple-factor analysis with logistic regression analysis was made to analyze the correlation between risk factors and mortality. RESULTS: The 60-day mortality was 34.7% (34/98). The APACHE II score of the death group was higher than that of the survival group (17.4±4.3 vs. 14.2±4.8, P<0.05). The mortality of the patients with a high level of cystatin C>1.3 mg/L was higher than that of the patients with a low level of cystatin C (<1.3 mg/L) (50% vs. 20%, P<0.05). The univariate analysis indicated that organ failures≥2, oliguria, APACHE II>15 scores, cystatin C>1.3 mg/L, cystatin C>1.3 mg/L+APACHE II>15 scores were the risk factors of AKI. Logistic regression analysis, however, showed that organ failures≥2, oliguria, cystatin C>1.3 mg/L +APACHE II>15 scores were the independent risk factors of AKI. CONCLUSION: Cystatin C>1.3 mg/L+APACHE II>15 scores is useful in predicting adverse clinical outcomes in patients with AKI.

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