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Updated: Jan 23, 2026

A Zebrafish Model of Diabetes Mellitus and Metabolic Memory
Published on: February 28, 2013
Caspase/AIF/apoptosis pathway: a new target of puerarin for diabetes mellitus therapy
Tao Liang1, Xiaohui Xu2, Dongmei Ye3
1College of Stomatology of Guangxi Medical University, No. 10, Shuangyong Road, Nanning, 530021, People's Republic of China. kqliangtao@126.com.
Abstract:
Pancreatic β cell damage is one of the crucial factors responsible for the development of type 2 diabetes mellitus (T2DM). Previous studies have suggested that puerarin (PR) could regulate the activities of the mitochondrial respiratory chain complex in diabetic nephropathy (DN); however, whether PR can inhibit pancreatic β-cell apoptosis in T2DM remains to be elucidated. In the present study, T2DM mice induced by high-fat diet and streptozotocin (STZ) injection were used as a working model to investigate the mechanism of PR on pancreatic β cell apoptosis. The results showed that PR decreased the serum fasting blood glucose (FBG), total cholesterol (TC), triglyceride (TG) and low-density lipoprotein (LDL) levels but significantly increased the fasting blood insulin (FINS) and high-density lipoprotein (HDL) levels. Furthermore, decreased caspase-3, 8, 9 and apoptosis-inducing factor (AIF) proteins in the pancreas were detected by Western blot analysis. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) staining demonstrated that the pancreatic β cell apoptosis was inhibited by PR. Furthermore, PR improved the histopathological changes in pancreatic tissue in T2DM mice. Collectively, the data show that PR can protect the β cells from apoptotic death in a mouse model of T2DM through regulating the expression of apoptosis-related protein-AIF and caspase family proteins.
Insights
Puerarin (PR) protects pancreatic beta cells from apoptosis in type 2 diabetes mellitus (T2DM) mice. This study shows PR reduces blood glucose and improves insulin levels by regulating apoptosis-related proteins.
Area of Science:
- Endocrinology
- Cell Biology
- Pharmacology
Background:
- Pancreatic beta cell damage is a key factor in type 2 diabetes mellitus (T2DM) development.
- Puerarin (PR) has shown potential in regulating mitochondrial function in diabetic nephropathy.
- The effect of PR on pancreatic beta cell apoptosis in T2DM requires further investigation.
Purpose of the Study:
- To investigate the protective mechanism of Puerarin (PR) against pancreatic beta cell apoptosis in a mouse model of type 2 diabetes mellitus (T2DM).
Main Methods:
- Type 2 diabetes mellitus (T2DM) was induced in mice using a high-fat diet and streptozotocin (STZ).
- Mice were treated with Puerarin (PR) to assess its effects on glycemic control and pancreatic beta cell apoptosis.
- Western blot analysis and TUNEL staining were employed to evaluate apoptosis-related protein expression and cell death.
Main Results:
- Puerarin (PR) treatment significantly reduced fasting blood glucose (FBG), total cholesterol (TC), triglyceride (TG), and LDL levels.
- PR treatment increased fasting insulin (FINS) and HDL levels.
- PR inhibited pancreatic beta cell apoptosis by downregulating caspase-3, 8, 9, and apoptosis-inducing factor (AIF) protein expression, and improved pancreatic histopathology.
Conclusions:
- Puerarin (PR) demonstrates protective effects against pancreatic beta cell apoptosis in a T2DM mouse model.
- PR exerts its protective effects by modulating the expression of key apoptosis-related proteins, including the caspase family and AIF.
- These findings suggest Puerarin (PR) as a potential therapeutic agent for T2DM by preserving beta cell function.
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