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2.
Int J Med Sci ; 18(16): 3831-3838, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34790059

RESUMO

Fas-induced apoptosis is a central mechanism of hepatocyte damage during acute and chronic hepatic disorders. Increasing evidence suggests that circadian clock plays critical roles in the regulation of cell fates. In the present study, the potential significance of REV-ERBα, a core ingredient of circadian clock, in Fas-induced acute liver injury has been investigated. The anti-Fas antibody Jo2 was injected intraperitoneally in mice to induce acute liver injury and the REV-ERBα agonist GSK4112 was administered. The results indicated that treatment of GSK4112 decreased the level of plasma ALT and AST, attenuated the liver histological changes, and promoted the survival rate in Jo2-insulted mice. Treatment with GSK4112 also downregulated the activities of caspase-3 and caspase-8, suppressed hepatocyte apoptosis. In addition, treatment with GSK4112 decreased the level of Fas and enhanced the phosphorylation of Akt. In conclusion, treatment with GSK4112 alleviated Fas-induced apoptotic liver damage in mice, suggesting that REV-ERBα agonist might have potential value in pharmacological intervention of Fas-associated liver injury.

4.
Nanoscale ; 13(40): 17168-17182, 2021 Oct 21.
Artigo em Inglês | MEDLINE | ID: mdl-34636386

RESUMO

Light-stimulus-responsive therapies have been recognized as a promising strategy for the efficient and safe treatment of oral squamous cell carcinoma (OSCC). Hydrogels have emerged as a promising multifunctional platform combining localized drug delivery and sustained drug release with multimodal properties for combined OSCC therapy. However, inaccurate drug release and limited light-absorption efficiency have hindered their on-demand chemo-photothermal applications. To tackle these problems, an injectable and near-infrared (NIR) light-responsive hybrid system was developed by incorporating light-responsive mesoporous silica nanoparticles (MSNs) as doxorubicin (DOX) carriers into the IR820/methylcellulose hydrogel networks for chemophotothermal therapy. Under NIR radiation, the incorporated IR820, a new green cyanine dye, was excited to induce photothermal effects against tumor cells. Meanwhile, MSNs achieved self-degradation-controlled DOX release via the cleavage of diselenide bonds induced by reactive oxygen species. Through the combination of chemotherapy and phototherapy, a long-lasting synergistic anti-tumor effect was achieved in vitro and in vivo with less toxicity. These findings demonstrate the potential of light-responsive hydrogels as a multifunctional platform for accurate synergistic chemophotothermal treatment of OSCC.


Assuntos
Carcinoma de Células Escamosas , Hipertermia Induzida , Neoplasias Bucais , Nanopartículas , Carcinoma de Células Escamosas/tratamento farmacológico , Doxorrubicina/farmacologia , Liberação Controlada de Fármacos , Humanos , Hidrogéis , Raios Infravermelhos , Neoplasias Bucais/tratamento farmacológico , Fototerapia , Terapia Fototérmica
5.
Theranostics ; 11(19): 9198-9216, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34646366

RESUMO

Small extracellular vesicles (sEVs) operate as a signaling platform due to their ability to carry functional molecular cargos. However, the role of sEVs in hypoxic tumor microenvironment-mediated premetastatic niche formation remains poorly understood. Methods: Protein expression profile of sEVs derived from normoxic and hypoxic head and neck squamous cell carcinoma (HNSCC) cells were determined by Isobaric Tagging Technology for Relative Quantitation. In vitro invasion assay and in vivo colonization were performed to evaluate the role of sEV-delivering proteins. Results: We identified lysyl oxidase like 2 (LOXL2) which had the highest fold increase in hypoxic sEVs compared with normoxic sEVs. Hypoxic cell-derived sEVs delivered high amounts of LOXL2 to non-hypoxic HNSCC cells to elicit epithelial-to-mesenchymal transition (EMT) and induce the invasion of the recipient cancer cells. Moreover, LOXL2-enriched sEVs were incorporated by distant fibroblasts and activate FAK/Src signaling in recipient fibroblasts. Increased production of fibronectin mediated by FAK/Src signaling recruited myeloid-derived suppressor cells to form a premetastatic niche. Serum sEV LOXL2 can reflect a hypoxic and aggressive tumor type and can serve as an alternative to tissue LOXL2 as an independent prognostic factor of overall survival for patients with HNSCC. Conclusion: sEVs derived from the hypoxic tumor microenvironment of HNSCC can drive local invasion of non-hypoxic HNSCC cells and stimulate premetastatic niche formation by delivering LOXL2 to non-hypoxic HNSCC cells and fibroblasts to induce EMT and fibronectin production, respectively.

6.
Immunol Lett ; 240: 24-30, 2021 12.
Artigo em Inglês | MEDLINE | ID: mdl-34525396

RESUMO

The mitochondria are the primary source of reactive oxygen species (ROS) under pathological condition, but the significance of mitochondrial ROS in the development of Lipopolysaccharide (LPS)/D-galactosamine (D-Gal)-induced acute liver injury remains unclear. In the present study, the level of mitochondrial ROS in LPS/D-Gal has been determined by MitoSox staining and the potential roles of mitochondrial ROS in LPS/D-Gal-induced liver injury have been investigated by using the mitochondria-targeting antioxidant MitoQ. The results indicated that LPS/D-Gal exposure induced the generation of mitochondrial ROS while treatment with MitoQ reduced the level of mitochondrial ROS. Treatment with MitoQ ameliorated LPS/D-Gal-induced histopathologic abnormalities, suppressed the elevation of AST and ALT, and increased the survival rate of the experimental animals. Treatment with MitoQ also suppressed LPS/D-Gal-induced production of tumor necrosis factor α (TNF-α), inhibited the activities of caspase-3, caspase-8 and caspase-9, decreased the level of cleaved caspase-3 and reduced the counts of TUNEL positive cells. These results indicate that mitochondrial ROS is involved in the development of LPS-induced acute liver injury and the mitochondria-targeting antioxidant MitoQ might have potential value for the treatment of inflammation-based acute liver injury.

7.
J Hematol Oncol ; 14(1): 136, 2021 09 03.
Artigo em Inglês | MEDLINE | ID: mdl-34479611

RESUMO

Extracellular vesicles (EVs) are cell-derived membrane structures enclosing proteins, lipids, RNAs, metabolites, growth factors, and cytokines. EVs have emerged as essential intercellular communication regulators in multiple physiological and pathological processes. Previous studies revealed that mesenchymal stem cells (MSCs) could either support or suppress tumor progression in different cancers by paracrine signaling via MSC-derived EVs. Evidence suggested that MSC-derived EVs could mimic their parental cells, possessing pro-tumor and anti-tumor effects, and inherent tumor tropism. Therefore, MSC-derived EVs can be a cell-free cancer treatment alternative. This review discusses different insights regarding MSC-derived EVs' roles in cancer treatment and summarizes bioengineered MSC-derived EVs' applications as safe and versatile anti-tumor agent delivery platforms. Meanwhile, current hurdles of moving MSC-derived EVs from bench to bedside are also discussed.


Assuntos
Antineoplásicos/administração & dosagem , Sistemas de Liberação de Medicamentos , Vesículas Extracelulares/metabolismo , Células-Tronco Mesenquimais/citologia , Neoplasias/terapia , Animais , Antineoplásicos/uso terapêutico , Apoptose , Proliferação de Células , Vesículas Extracelulares/transplante , Humanos , Células-Tronco Mesenquimais/metabolismo , Neoplasias/metabolismo , Neoplasias/patologia
8.
Front Cell Infect Microbiol ; 11: 728933, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34485181

RESUMO

Introduction: The oral squamous cell carcinoma (OSCC) is detrimental to patients' physical and mental health. The prognosis of OSCC depends on the early diagnosis of OSCC in large populations. Objectives: Here, the present study aimed to develop an early diagnostic model based on the relationship between OSCC and oral microbiota. Methods: Overall, 164 samples were collected from 47 OSCC patients and 48 healthy individuals as controls, including saliva, subgingival plaque, the tumor surface, the control side (healthy mucosa), and tumor tissue. Based on 16S rDNA sequencing, data from all the five sites, and salivary samples only, two machine learning models were developed to diagnose OSCC. Results: The average diagnostic accuracy rates of five sites and saliva were 98.17% and 95.70%, respectively. Cross-validations showed estimated external prediction accuracies of 96.67% and 93.58%, respectively. The false-negative rate was 0%. Besides, it was shown that OSCC could be diagnosed on any one of the five sites. In this model, Actinobacteria, Fusobacterium, Moraxella, Bacillus, and Veillonella species exhibited strong correlations with OSCC. Conclusion: This study provided a noninvasive and inexpensive way to diagnose malignancy based on oral microbiota without radiation. Applying machine learning methods in microbiota data to diagnose OSCC constitutes an example of a microbial assistant diagnostic model for other malignancies.


Assuntos
Carcinoma de Células Escamosas , Neoplasias de Cabeça e Pescoço , Microbiota , Neoplasias Bucais , Biomarcadores Tumorais , Carcinoma de Células Escamosas/diagnóstico , Humanos , Neoplasias Bucais/diagnóstico , Saliva , Carcinoma de Células Escamosas de Cabeça e Pescoço
9.
Pharmacol Res ; 172: 105838, 2021 10.
Artigo em Inglês | MEDLINE | ID: mdl-34425230

RESUMO

Accumulating evidence indicates that metabolic events profoundly modulate the progression of various diseases. Pyruvate is a central metabolic intermediate in glucose metabolism. In the present study, the metabolic status of pyruvate and its pharmacological significance has been investigated in mice with lipopolysaccharide/D-galactosamine (LPS/D-Gal)-induced fulminant liver injury. Our results indicated that LPS/D-Gal exposure decreased the activity of pyruvate kinase and the content of pyruvate, which were reversed by the PKM2 activator TEPP-46. Pretreatment with TEPP-46 or supplementation with the cell-permeable pyruvate derivate ethyl pyruvate (EP) attenuated LPS/D-Gal-induced liver damage. Interestingly, post-insult intervention of pyruvate metabolism also resulted in beneficial outcomes. The phospho-antibody microarray analysis and immunoblot analysis found that the inhibitory phosphorylation of cyclin dependent kinase 1 (CDK1) was reversed by TEPP-46, DASA-58 or EP. In addition, the therapeutic benefits of PKM2 activator or EP were blunted by the CDK1 inhibitor Ro 3306. Our data suggests that LPS/D-Gal exposure-induced decline of pyruvate might be a novel metabolic mechanism underlies the development of LPS/D-Gal-induced fulminant liver injury, PKM2 activator or pyruvate derivate might have potential value for the pharmacological intervention of fulminant liver injury.

10.
Biomolecules ; 11(8)2021 07 31.
Artigo em Inglês | MEDLINE | ID: mdl-34439795

RESUMO

The cranial bones constitute the protective structures of the skull, which surround and protect the brain. Due to the limited repair capacity, the reconstruction and regeneration of skull defects are considered as an unmet clinical need and challenge. Previously, it has been proposed that the periosteum and dura mater provide reparative progenitors for cranial bones homeostasis and injury repair. In addition, it has also been speculated that the cranial mesenchymal stem cells reside in the perivascular niche of the diploe, namely, the soft spongy cancellous bone between the interior and exterior layers of cortical bone of the skull, which resembles the skeletal stem cells' distribution pattern of the long bone within the bone marrow. Not until recent years have several studies unraveled and validated that the major mesenchymal stem cell population of the cranial region is primarily located within the suture mesenchyme of the skull, and hence, they are termed suture mesenchymal stem cells (SuSCs). Here, we summarized the characteristics of SuSCs, this newly discovered stem cell population of cranial bones, including the temporospatial distribution pattern, self-renewal, and multipotent properties, contribution to injury repair, as well as the signaling pathways and molecular mechanisms associated with the regulation of SuSCs.


Assuntos
Regeneração Óssea/genética , Suturas Cranianas/citologia , Células-Tronco Mesenquimais/citologia , Osteócitos/citologia , Fraturas Cranianas/genética , Animais , Proteína Axina/genética , Proteína Axina/metabolismo , Catepsina K/genética , Catepsina K/metabolismo , Diferenciação Celular , Proliferação de Células , Suturas Cranianas/crescimento & desenvolvimento , Suturas Cranianas/lesões , Suturas Cranianas/metabolismo , Craniossinostoses/genética , Craniossinostoses/metabolismo , Craniossinostoses/patologia , Regulação da Expressão Gênica , Proteínas de Homeodomínio/genética , Proteínas de Homeodomínio/metabolismo , Humanos , Células-Tronco Mesenquimais/metabolismo , Osteócitos/metabolismo , Transdução de Sinais , Fraturas Cranianas/metabolismo , Fraturas Cranianas/patologia , Proteína GLI1 em Dedos de Zinco/genética , Proteína GLI1 em Dedos de Zinco/metabolismo
11.
J Nutr Sci Vitaminol (Tokyo) ; 67(3): 145-152, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34193673

RESUMO

Acetaminophen (N-acetyl-p-aminophenol, APAP) overdose causes hepatotoxicity, even liver failure, and oxidative stress plays pivotal role in its pathogenesis. Nicotinic acid (NA) is one form of vitamin B3, which has been used to treat a series of diseases in clinic for decades. To date, several studies have evidenced that NA has anti-oxidative property. Therefore, NA may have the hepatoprotective potential against APAP-induced toxicity. Here, our aim was to investigate the beneficial effect of NA against hepatotoxicity induced by APAP and its mechanism in vivo. BALB/c mice were intraperitoneally injected with NA (100 mg/kg) 3 times at 24, 12 and 1 h before APAP (600 mg/kg or 400 mg/kg) challenge. The results showed that pretreatment of NA markedly improved the survival rate, alleviated serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels and mitigated the histopathological injuries compared to APAP-exposed mice. Furthermore, NA significantly elevated the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH) content, while reduced malondialdehyde (MDA) level. Finally, the signaling pathway was probed. The western blot revealed that NA up-regulated Sirtuin1 (Sirt1), nuclear factor erythroid 2-related factor 2 (Nrf2) and NAD(P)H quinone dehydrogenase-1 (NQO-1) expression and down-regulated Kelch-like ECH-associated protein 1 (Keap1) level in liver followed APAP exposure, implying Sirt1/Nrf2 axis exerted an essential role in the protective mechanism of NA on APAP toxicity. In brief, pretreatment of NA effectively protects liver against hepatotoxicity due to overdose of APAP through an antioxidant dependent manner modulated by Sirt1/Nrf2 signaling pathway.


Assuntos
Doença Hepática Induzida por Substâncias e Drogas , Niacina , Acetaminofen/metabolismo , Acetaminofen/toxicidade , Animais , Antioxidantes/metabolismo , Doença Hepática Induzida por Substâncias e Drogas/tratamento farmacológico , Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle , Proteína 1 Associada a ECH Semelhante a Kelch/metabolismo , Fígado/metabolismo , Camundongos , Camundongos Endogâmicos BALB C , Fator 2 Relacionado a NF-E2/metabolismo , Niacina/metabolismo , Estresse Oxidativo , Sirtuína 1/metabolismo
12.
Hua Xi Kou Qiang Yi Xue Za Zhi ; 39(2): 215-220, 2021 Apr 01.
Artigo em Chinês | MEDLINE | ID: mdl-33834678

RESUMO

Photodynamic therapy (PDT) has developed rapidly in basic and clinical research, and its therapeutic prospects have received increasing attention. PDT has the advantages of minimally invasive, low toxicity, high selectivity, good reproducibility, protection of appearance and vital organ function, and has become a treatment. With the development of medicine, the field of application of PDT becomes more wildly, and brings a new direction for the treatment of oral diseases. This article reviews the basic principles, treatment elements and research results of PDT in the treatment of oral diseases.


Assuntos
Doenças da Boca , Fotoquimioterapia , Humanos , Doenças da Boca/tratamento farmacológico , Fármacos Fotossensibilizantes/uso terapêutico , Reprodutibilidade dos Testes
13.
Hua Xi Kou Qiang Yi Xue Za Zhi ; 39(2): 221-226, 2021 Apr 01.
Artigo em Chinês | MEDLINE | ID: mdl-33834679

RESUMO

Bone invasion by oral cancer is a common clinical problem, which affects the choice of treatment and predicts a poor prognosis. Unfortunately, the molecular mechanism of this phenomenon has not been fully elucidated. Current studies have revealed that oral cancer cells modulate the formation and function of osteoclasts through the expression of a series of signal molecules. Many signal pathways are involved in this process, of which receptor activator of nuclear factor-κB ligand/receptor activator of nuclear factor-κB/osteoprotegerin signaling pathway attracted much attention. In this review, we introduce recent progress in molecular mechanisms of bone invasion by oral cancer.


Assuntos
Reabsorção Óssea , Neoplasias Bucais , Osso e Ossos , Humanos , Osteoclastos , Osteoprotegerina , Ligante RANK , Receptor Ativador de Fator Nuclear kappa-B
14.
Exp Anim ; 70(3): 302-310, 2021 Aug 06.
Artigo em Inglês | MEDLINE | ID: mdl-33678756

RESUMO

The metabolic sensor sirtuin 1 (SIRT1) also functions as a checkpoint in inflammation, and SRT1720 is a highly active and selective SIRT1 activator shown to alleviate inflammatory injury in several recent experimental studies. In the present study, the potential effects and underlying mechanisms of SRT1720 on lipopolysaccharide (LPS)-induced fulminant hepatitis in D-galactosamine (D-Gal)-sensitized mice were investigated. The results indicated that treatment with SRT1720 inhibited LPS/D-Gal-induced elevation of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), alleviated the histological abnormalities, suppressed the induction of tumor necrosis factor alpha (TNF-α) and IL-6, mitigated the phosphorylation of c-Jun N-terminal kinase (JNK), downregulated the activities of caspase 8, caspase 9 and caspase 3, decreased the level of cleaved caspase 3, reduced the TUNEL-positive cells, and improved the survival rate of the LPS/D-Gal-exposed mice. These data indicated that treatment with the SIRT1 activator SRT1720 alleviated LPS/D-Gal-induced fulminant hepatitis, which might be attributed to the suppressive effects of SRT1720 on TNF-α production and the subsequent activation of the apoptosis cascade.


Assuntos
Apoptose/fisiologia , Compostos Heterocíclicos de 4 ou mais Anéis/farmacologia , Longevidade/efeitos dos fármacos , Necrose Hepática Massiva/prevenção & controle , Substâncias Protetoras/farmacologia , Sirtuína 1/metabolismo , Animais , Hepatócitos/fisiologia , Inflamação/prevenção & controle , Masculino , Camundongos , Camundongos Endogâmicos BALB C
16.
Int J Oral Sci ; 13(1): 10, 2021 03 22.
Artigo em Inglês | MEDLINE | ID: mdl-33753723

RESUMO

C18 ceramide plays an important role in the occurrence and development of oral squamous cell carcinoma. However, the function of ceramide synthase 1, a key enzyme in C18 ceramide synthesis, in oral squamous cell carcinoma is still unclear. The aim of our study was to investigate the relationship between ceramide synthase 1 and oral cancer. In this study, we found that the expression of ceramide synthase 1 was downregulated in oral cancer tissues and cell lines. In a mouse oral squamous cell carcinoma model induced by 4-nitroquinolin-1-oxide, ceramide synthase 1 knockout was associated with the severity of oral malignant transformation. Immunohistochemical studies showed significant upregulation of PCNA, MMP2, MMP9, and BCL2 expression and downregulation of BAX expression in the pathological hyperplastic area. In addition, ceramide synthase 1 knockdown promoted cell proliferation, migration, and invasion in vitro. Overexpression of CERS1 obtained the opposite effect. Ceramide synthase 1 knockdown caused endoplasmic reticulum stress and induced the VEGFA upregulation. Activating transcription factor 4 is responsible for ceramide synthase 1 knockdown caused VEGFA transcriptional upregulation. In addition, mild endoplasmic reticulum stress caused by ceramide synthase 1 knockdown could induce cisplatin resistance. Taken together, our study suggests that ceramide synthase 1 is downregulated in oral cancer and promotes the aggressiveness of oral squamous cell carcinoma and chemotherapeutic drug resistance.


Assuntos
Carcinoma de Células Escamosas , Neoplasias de Cabeça e Pescoço , Neoplasias Bucais , Animais , Apoptose , Linhagem Celular Tumoral , Regulação para Baixo , Estresse do Retículo Endoplasmático , Camundongos , Oxirredutases
17.
Hua Xi Kou Qiang Yi Xue Za Zhi ; 39(1): 99-104, 2021 Feb 01.
Artigo em Inglês, Chinês | MEDLINE | ID: mdl-33723944

RESUMO

Oral squamous cell carcinoma (OSCC) is the most frequent tumour in head and neck malignant. The current treatment is mainly based on surgery therapy, radiation therapy and chemical therapy. Meanwhile, there are many a defect in the treatment. For example, there are many defects in radiotherapy. Radioactive salivatitis is the most common. In addition, there are a series of changes such as dry mouth, oral mucositis, rampant dental caries, and radioactive osteomyelitis of jaw, which cause swallowing, chewing problems, and taste dysfunction. Currently, the research on radioactive salivatitis is progressing rapidly, but its mechanism is more complication. This paper review aims to summarize the research progress in this field.


Assuntos
Carcinoma de Células Escamosas , Cárie Dentária , Neoplasias de Cabeça e Pescoço , Neoplasias Bucais , Lesões por Radiação , Xerostomia , Neoplasias de Cabeça e Pescoço/radioterapia , Humanos , Glândulas Salivares , Xerostomia/etiologia
18.
Innate Immun ; 27(2): 201-209, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-33576722

RESUMO

Increasing evidence indicates that signal transducer and activator of transcription 3 (STAT3), a vital transcription factor, plays crucial roles in the regulation of inflammation. STAT3 has become a novel therapeutic target for intervention in inflammation-related disorders. However, it remains unclear whether STAT3 plays a part in acute hepatic damage. To investigate the effects of STAT3 here, LPS/d-GalN-induced hepatic damage was induced in mice, the STAT3 inhibitor Stattic was administered, and the degree of liver injury, inflammation, and hepatocyte apoptosis were investigated. The results showed that Stattic mitigated the hepatic morphologic abnormalities and decreased the level of aminotransferase in LPS/D-GalN-insulted mice. The results also indicated that Stattic decreased the levels of TNF-α and IL-6, prevented the activation of the caspase cascade, suppressed cleavage of PARP, and decreased the quantity of TUNEL-positive cells. These results suggest that Stattic provided protective benefits in LPS/d-GalN-induced hepatic damage, and the protective effects might be associated with its anti-inflammatory and anti-apoptotic effects. Therefore, STAT3 might become a novel target for intervening in inflammation-based and apoptosis-based hepatic disorders.

19.
Cancer Lett ; 506: 11-22, 2021 05 28.
Artigo em Inglês | MEDLINE | ID: mdl-33639203

RESUMO

The mechanisms underlying the hypoxic cancer cell-mediated differentiation of cancer-associated fibroblasts (CAFs) have not been elucidated yet. The present study showed that the hypoxic head and neck squamous cell carcinoma (HNSCC) cells promoted CAF-like differentiation through secreting TGF-ß and small extracellular vesicles (sEVs) that contain enhanced levels of miR-192/215 family miRNAs. Caveolin-1 (CAV1), which is a target gene of miR-192/215, inhibited the TGF-ß/SMAD signaling and promoted CAF-like differentiation of the fibroblasts. Restoring the levels of CAV1 inhibited the hypoxic sEV- and TGF-ß-induced CAF-like differentiation. The enhanced levels of miR-192/215 encapsulated in the HNSCC tissue-derived sEVs (but not serum-derived sEVs) indicated hypoxic and aggressive cancer stroma. miR-215 in the tumor tissue-derived sEVs (but not circulating sEVs) was correlated with poor overall survival of patients with HNSCC. This study demonstrated that sEVs function as a "courier" to deliver miRNAs from the cancer cells to the fibroblasts, which promotes the remodeling of the hypoxic tumor microenvironment, and that cancer tissue-derived sEV could potentially serve as a source of biomarker.


Assuntos
Fibroblastos Associados a Câncer/citologia , Vesículas Extracelulares/fisiologia , Neoplasias de Cabeça e Pescoço/patologia , MicroRNAs/fisiologia , Carcinoma de Células Escamosas de Cabeça e Pescoço/patologia , Hipóxia Tumoral/fisiologia , Caveolina 1/fisiologia , Diferenciação Celular , Linhagem Celular Tumoral , Progressão da Doença , Humanos
20.
Diabetes Ther ; 12(5): 1249-1278, 2021 May.
Artigo em Inglês | MEDLINE | ID: mdl-33481189

RESUMO

INTRODUCTION: The question of whether periodontal therapy is an effective strategy for achieving glycemic control in people with type 2 diabetes mellitus (T2DM) and periodontitis continues to be open to debate. To clarify this issue, we conducted a systematic review and meta-analysis. METHODS: A systematic literature search of randomized controlled trials (RCTs) was carried out by searching four electronic databases and four journals up to April 2020. RCTs that evaluated the effect of periodontal therapy on glycemic control in people with T2DM were included. RESULTS: A total of 23 RCTs were included in this systematic review and meta-analysis. We found that after 3 and 6 months, periodontal therapy could significantly reduce glycosylated hemoglobin (HbA1c) level (3-month: weighted mean difference [WMD] - 0.514, 95% confidence interval [CI] - 0.730, - 0.298, p = 0.000; 6-month: WMD - 0.548, 95% CI - 0.859, - 0.238, p = 0.000). However, huge heterogeneity existed. Further analyses on 11 potential sources of heterogeneity found that baseline HbA1c of the included studies was the most significant factor causing heterogeneity. The benefit of periodontal therapy on glycemic control was much more obvious in studies with a higher baseline HbA1c level than in those with a lower baseline HbA1c level. CONCLUSIONS: Periodontal therapy significantly contributed to glycemic control in T2DM patients, especially in patients with higher baseline HbA1c level.

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