Background:To investigate the pharmacological effects of Fangshi Jiangtang decoction(FSJT)on type 2 diabetes mellitus(T2DM)model rats and explore its mechanism of action from the perspective of mitochondrial autophagy...Background:To investigate the pharmacological effects of Fangshi Jiangtang decoction(FSJT)on type 2 diabetes mellitus(T2DM)model rats and explore its mechanism of action from the perspective of mitochondrial autophagy.Methods:Sixty Sprague Dawley rats were randomly divided into six groups after one week of adaptive feeding:Control group,T2DM model group,metformin group(0.2 g/kg by gavage),and FSJT low,medium,and high dose groups(9.5,19,38 g/kg by gavage).Except for the Control group,the other five groups were given a high-fat diet.The treatment lasted for 8 weeks,and blood glucose levels were measured weekly.Eight weeks later,blood samples were collected from the rats,and serum was separated for the determination of HbA1c,oral glucose tolerance test,and homeostatic model assessment for insulin resistance index.The pancreas of the rats was collected,weighed,and fixed.The same part of the pancreas was used for hematoxylin-eosin.Kits were used to detect triglycerides,total cholesterol,interleukin-1β,interleukin-6,tumor necrosis factor-α,malondialdehyde,glutathione peroxidase,and superoxide dismutase in pancreatic tissue to assess the effects of FSJT on inflammation and oxidative stress in T2DM rats.Western blot analysis was performed to detect the expression of VDAC1,TOM20,COXⅣ,PINK1,Parkin,beclin1,light chain 3,and selective autophagy adaptor protein P62 to evaluate the effects of FSJT on mitochondrial autophagy in T2DM model rats.Results:Compared with the T2DM model group,FSJT intervention significantly reduced blood glucose,HbA1c,oral glucose tolerance test,and homeostatic model assessment for insulin resistance index in T2DM model rats,alleviated pancreatic tissue lesions,reduced levels of total cholesterol,triglycerides,interleukin-1β,interleukin-6,tumor necrosis factor-α,and malondialdehyde,increased glutathione peroxidase and superoxide dismutase activities,downregulated the expression of VDAC1,TOM20,COXⅣ,and P62 proteins,and upregulated the expression of PINK1,Parkin,Beclin1,and light chain 3 proteins.Conclusion:FSJT can improve insulin resistance in T2DM by promoting the activation of mitochondrial autophagy.展开更多
基金supported by Applied Basic Research Project of Jiaxing Science and Technology Bureau(2023AD11047)the Joint Project of Yunnan Provincial Science and Technology Department and Yunnan University of Chinese Medicine(202101AZ070001-064).
文摘Background:To investigate the pharmacological effects of Fangshi Jiangtang decoction(FSJT)on type 2 diabetes mellitus(T2DM)model rats and explore its mechanism of action from the perspective of mitochondrial autophagy.Methods:Sixty Sprague Dawley rats were randomly divided into six groups after one week of adaptive feeding:Control group,T2DM model group,metformin group(0.2 g/kg by gavage),and FSJT low,medium,and high dose groups(9.5,19,38 g/kg by gavage).Except for the Control group,the other five groups were given a high-fat diet.The treatment lasted for 8 weeks,and blood glucose levels were measured weekly.Eight weeks later,blood samples were collected from the rats,and serum was separated for the determination of HbA1c,oral glucose tolerance test,and homeostatic model assessment for insulin resistance index.The pancreas of the rats was collected,weighed,and fixed.The same part of the pancreas was used for hematoxylin-eosin.Kits were used to detect triglycerides,total cholesterol,interleukin-1β,interleukin-6,tumor necrosis factor-α,malondialdehyde,glutathione peroxidase,and superoxide dismutase in pancreatic tissue to assess the effects of FSJT on inflammation and oxidative stress in T2DM rats.Western blot analysis was performed to detect the expression of VDAC1,TOM20,COXⅣ,PINK1,Parkin,beclin1,light chain 3,and selective autophagy adaptor protein P62 to evaluate the effects of FSJT on mitochondrial autophagy in T2DM model rats.Results:Compared with the T2DM model group,FSJT intervention significantly reduced blood glucose,HbA1c,oral glucose tolerance test,and homeostatic model assessment for insulin resistance index in T2DM model rats,alleviated pancreatic tissue lesions,reduced levels of total cholesterol,triglycerides,interleukin-1β,interleukin-6,tumor necrosis factor-α,and malondialdehyde,increased glutathione peroxidase and superoxide dismutase activities,downregulated the expression of VDAC1,TOM20,COXⅣ,and P62 proteins,and upregulated the expression of PINK1,Parkin,Beclin1,and light chain 3 proteins.Conclusion:FSJT can improve insulin resistance in T2DM by promoting the activation of mitochondrial autophagy.
