Epigallocatechin-3-gallate protects pro-inflammatory cytokine induced injuries in insulin-producing cells through the mitochondrial pathway

Zhang, Zhaofeng; Ding, Ye; Dai, Xiaoqian; Wang, Junbo; Li, Yong

doi:10.1016/j.ejphar.2011.08.033

Cited by 74 publications

(50 citation statements)

References 31 publications

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“…In the present study, the in vitro model of cytokine-induced pancreatic b-cell death was established. In the study of Delaney et al, 20 In this study, we observed that a 3-day exposure of the same dosages of cytokines severely impaired RIN-m5f b cells and induced cell apoptosis. The cytotoxic effects of cytokines on b cells might depend on their concentrations, duration of exposure, and cell types.…”

Section: Discussionmentioning

confidence: 52%

“…To induce b-cell death, cells were challenged for 3 days with the same dosages of cytokines (10 ng/mL TNF-a, 5 ng/mL IL-1b, and 1000 IU/ mL IFN-c [herein referred to as TII]) used in the recent study from this laboratory. 20 In this set of experiments, cells were pretreated with different doses of myricetin for 3 h prior to TII stimulation and continuously treated with TII and different doses of myricetin. All of the determinations were performed 3 days later.…”

Section: Cell Culturementioning

confidence: 99%

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Myricetin Protects Against Cytokine-Induced Cell Death in RIN-m5f β Cells

Ding

Zhang

Dai

et al. 2012

Journal of Medicinal Food

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Cytokine-induced cell death is recognized as a major cause of progressive b-cell loss. Tumor necrosis factor a (TNF-a), interleukin 1b (IL-1b), and interferon c (IFN-c) in combination trigger a series of events that lead to b-cell death. In the past few decades, the use of myricetin as an anti-inflammatory and cytoprotective agent has gained much attention. The present study focused on the protective roles of myricetin against cytokine-induced cell death in insulin-secreting RIN-m5f b cells. The results showed that myricetin (especially at concentrations of 10 lM and 20 lM) increased cell viability and decreased cell apoptosis induced by the cytokine mixture of TNF-a (10 ng/mL), IL-1b (5 ng/mL), and IFN-c (1000 IU/mL) for 3 days. Moreover, the cytokines increased the total and p65 subunit levels of nuclear factor jB, decreased inhibitor jB a levels, stimulated the accumulation of nitric oxide, increased cytochrome c release from mitochondria, and induced reactive oxygen species generation; myricetin (especially at the concentration of 20 lM) abolished all of these parameters. These results suggest that myricetin might have therapeutic value for preventing b-cell death.KEY WORDS: cytokines mitochondrial death pathway myricetin nuclear factor jB RIN-m5f b cells

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Section: Discussionmentioning

confidence: 52%

Section: Cell Culturementioning

confidence: 99%

Myricetin Protects Against Cytokine-Induced Cell Death in RIN-m5f β Cells

Ding

Zhang

Dai

et al. 2012

Journal of Medicinal Food

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“…EGCG was also shown to protect insulin-producing β-cells from pro-inflammatory cytokine-induced cytotoxicity, where treatment with EGCG partially restored glucose-stimulated insulin secretion (GSIS) and preserved cell viability [24]. Bcl-2 protein prevents oxidative stress and regulates mitochondrial transitional pore opening by opposing the effect of Bax thereby blocking cytochrome c release and inhibiting caspase activity [24–26].…”

Section: Flavonoidsmentioning

confidence: 99%

Recent advances in understanding the anti-diabetic actions of dietary flavonoids

Babu

Liu

Gilbert

2013

The Journal of Nutritional Biochemistry

471

313

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Flavonoids are polyphenolic compounds that are abundant in fruits and vegetables and increasing evidence demonstrates a positive relationship between consumption of flavonoid-rich foods and disease prevention. Epidemiological, in vitro and animal studies support the beneficial effects of dietary flavonoids on glucose and lipid homeostasis. It is encouraging that the beneficial effects of some flavonoids are at physiological concentrations and comparable to clinically-used anti-diabetic drugs; however, clinical research in this field and studies on the anti-diabetic effects of flavonoid metabolites are limited. Flavonoids act on various molecular targets and regulate different signaling pathways in pancreatic β-cells, hepatocytes, adipocytes, and skeletal myofibers. Flavonoids may exert beneficial effects in diabetes by (i) enhancing insulin secretion and reducing apoptosis and promoting proliferation of pancreatic β-cells, (ii) improving hyperglycemia through regulation of glucose metabolism in hepatocytes, (iii) reducing insulin resistance, inflammation and oxidative stress in muscle and fat, and (iv) increasing glucose uptake in skeletal muscle and white adipose tissue. This review highlights recent findings on the anti-diabetic effects of dietary flavonoids, including flavan-3-ols, flavanones, flavonols, anthocyanidins, flavones, and isoflavones, with particular emphasis on the studies that investigated the cellular and molecular mechanisms involved in the beneficial effects of the compounds.

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“…Similarly, the positive effects of EGCG on IR in dexamethasone-induced rat L6 cells was essentially dependent on the AMPK and PI3K/Akt activation pathway [22], while in differentiated rat L6 myotubes, EGCG and epicatechin enhanced insulin-mediated glucose uptake in vitro and translocation of glucose transporter (GLUT) 4 [23]. EGCG has also been shown to protect insulin-producing β-cells from pro-inflammatory cytokine-induced cytotoxicity via the modulation of B cell CLL/lymphoma 2 (BCL-2) expression [24]. …”

Section: Effects Of Nutrients On Gene Expression In the Pathogenesmentioning

confidence: 99%

Gene-Diet Interactions in Type 2 Diabetes: The Chicken and Egg Debate

Ortega

Berná

Rojas

et al. 2017

IJMS

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Consistent evidence from both experimental and human studies indicates that Type 2 diabetes mellitus (T2DM) is a complex disease resulting from the interaction of genetic, epigenetic, environmental, and lifestyle factors. Nutrients and dietary patterns are important environmental factors to consider in the prevention, development and treatment of this disease. Nutritional genomics focuses on the interaction between bioactive food components and the genome and includes studies of nutrigenetics, nutrigenomics and epigenetic modifications caused by nutrients. There is evidence supporting the existence of nutrient-gene and T2DM interactions coming from animal studies and family-based intervention studies. Moreover, many case-control, cohort, cross-sectional cohort studies and clinical trials have identified relationships between individual genetic load, diet and T2DM. Some of these studies were on a large scale. In addition, studies with animal models and human observational studies, in different countries over periods of time, support a causative relationship between adverse nutritional conditions during in utero development, persistent epigenetic changes and T2DM. This review provides comprehensive information on the current state of nutrient-gene interactions and their role in T2DM pathogenesis, the relationship between individual genetic load and diet, and the importance of epigenetic factors in influencing gene expression and defining the individual risk of T2DM.

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Epigallocatechin-3-gallate protects pro-inflammatory cytokine induced injuries in insulin-producing cells through the mitochondrial pathway

Cited by 74 publications

References 31 publications

Myricetin Protects Against Cytokine-Induced Cell Death in RIN-m5f β Cells

Myricetin Protects Against Cytokine-Induced Cell Death in RIN-m5f β Cells

Recent advances in understanding the anti-diabetic actions of dietary flavonoids

Gene-Diet Interactions in Type 2 Diabetes: The Chicken and Egg Debate

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