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Quercetin protects islet β-cells from oxidation-induced apoptosis via Sirt3 in T2DM

Jian-Yun Wang1, Ya-Xing Nie1, Bing-Zheng Dong2

  • 1Jiangsu Key Laboratory of New Drug Research and Clinical Pharmacy, Xuzhou Medical University, Xuzhou 221002, Jiangsu, PR China.

Iranian Journal of Basic Medical Sciences
|July 12, 2021
PubMed
Abstract

Insights

Quercetin protects against type 2 diabetes by preventing islet beta-cell apoptosis through Sirt3. This antioxidant action reduces oxidative stress and improves insulin levels in diabetic models.

Area of Science:

  • Endocrinology
  • Cell Biology
  • Biochemistry

Background:

  • Type 2 diabetes mellitus (T2DM) progression involves beta-cell apoptosis.
  • Sirtuin 3 (Sirt3) may regulate reactive oxygen species (ROS) production and beta-cell apoptosis.
  • Quercetin, an antioxidant bioflavonoid, has potential but unexplored effects on T2DM.

Purpose of the Study:

  • Investigate quercetin's effects on beta-cell apoptosis in T2DM.
  • Elucidate the underlying mechanisms of quercetin's action.

Main Methods:

  • Quercetin treatment in db/db mice and INS1 cells.
  • Measurement of blood glucose, serum insulin, and key proteins (Sirt3, SOD2, CAT, cleaved Caspase-3, Bax, BCL-2) via western blotting and ELISA.
  • Sirt3 knockdown in INS1 cells to assess its role.

Main Results:

  • Quercetin increased SOD2, CAT, and Sirt3 protein levels.
  • Quercetin decreased cleaved Caspase-3 and the Bax/BCL-2 ratio, reducing apoptosis.
  • Quercetin lowered blood glucose and increased insulin levels in diabetic mice.
  • Sirt3 knockdown abrogated quercetin's antioxidant and anti-apoptotic effects.

Conclusions:

  • Quercetin protects islet beta-cells from oxidation-induced apoptosis in T2DM via Sirt3.
  • This mechanism suggests quercetin's potential for new therapeutic strategies against T2DM-related beta-cell failure.
Keywords:
ApoptosisOxidative stressQuercetinSirt3β-cell

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