Jiangtang Sanhuang tablet inhibits endoplasmic reticulum stress and autophagy in diabetic mouse islet cells.
10.12122/j.issn.1673-4254.2022.09.07
- Author:
Wen Jing ZHANG
1
;
Zhao Xia HU
1
Author Information
1. Health Management Center, Third Affiliated Hospital, Southern Medical University, Guangzhou 510000, China.
- Publication Type:Randomized Controlled Trial, Veterinary
- Keywords:
Jiangtang Sanhuang tablets;
autophagy;
diabetes;
endoplasmic reticulum stress;
islet cells
- MeSH:
Animals;
Anthracenes;
Apoptosis;
Autophagy;
Blood Glucose;
Diabetes Mellitus;
Drinking Water;
Drugs, Chinese Herbal;
Endoplasmic Reticulum Stress;
Glucose/pharmacology*;
Glycolipids/pharmacology*;
Islets of Langerhans;
Metformin;
Mice;
Mice, Inbred C57BL;
Palmitic Acid/pharmacology*;
Tablets/pharmacology*
- From:
Journal of Southern Medical University
2022;42(9):1317-1323
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate effects of Jiangtang Sanhuang tablet (JTSHT) for regulating blood glucose and alleviating islet cell damage in db/db mice and its protective effects against endoplasmic reticulum stress (ERS) and autophagy induced by glycolipid toxicity.
METHODS:Forty db/db mice were randomized into 4 groups for daily intragastric administration of saline, JTSHT of 2.64 and 1.32 g/kg, and metformin at 0.225g/kg for 8 weeks, using 10 C57BL/6J mice as the normal control. After the treatments, the metabolic indexes of the mice were measured, and morphological changes of the islet cells were observed. A mouse islet cell line (MIN6) was exposed to high glucose (22 mmol/L glucose) and 0.1 mmol/L palmitic acid, followed by treatment with the sera from JTSHT- or saline- treated SD rats, alone or in combination with SP600125, and the changes in cell apoptosis, ERS and autophagy were evaluated using flow cytometry, RT-qPCR and Western blotting.
RESULTS:In db/db mice, treatment with JTSHT significantly improved glucose and lipid metabolism (P < 0.05) and suppressed progressive weight gain (P < 0.05) without significant effect on drinking water volume (P > 0.05). JTSHT was also found to promote repair of islet cell injuries. In the cell experiments, high glucose exposure significantly increased apoptosis rate of MIN6 cells (P < 0.05), which was obviously lowered by treatment with JTSHT-treated rat serum (P < 0.05). Western blotting showed that JTSHT significantly reduced the level of ERS and autophagy caused by glycolipid toxicity in MIN6 cells (P < 0.05). Interference with ERS using SP600125 significantly attenuated the protective effect of JTSHT against MIN6 cell injury, apoptosis and autophagy induced by glycolipid toxicity (P < 0.05).
CONCLUSION:JTSHT has protective effects against glycolipid toxicity in MIN6 cells possibly by inhibiting ERS and autophagy.
