Effect and mechanism of Tangzhi formula in improving glucose and lipid metabolism in type 2 diabetic rats
- VernacularTitle:糖止方对2型糖尿病大鼠糖脂代谢的改善作用及机制
- Author:
Jing CHEN
1
;
Min BAI
1
;
Fubin SHANG
2
;
Runsheng YU
2
;
Yan SU
3
;
Jianfeng WANG
4
;
Xiangdong ZHU
2
Author Information
1. College of Traditional Chinese Medicine，Ningxia Medical University，Yinchuan 750004，China;Key Laboratory of TCM Dryness Syndrome，Ministry of Education，Ningxia Medical University，Yinchuan 750004，China
2. College of Traditional Chinese Medicine，Ningxia Medical University，Yinchuan 750004，China
3. Dept. of Endocrine Diabetes，Ningxia Hui Autonomous Region Hospital of Traditional Chinese Medicine and Institute of Traditional Chinese Medicine，Yinchuan 750004，China
4. Periodical Press of Henan University of Chinese Medicine，Zhengzhou 450046，China
- Publication Type:Journal Article
- Keywords:
Tangzhi formula;
Type 2 diabetes mellitus;
glucose and lipid metabolism disorders;
PPAR signaling pathway;
hepatic lipid deposition
- From:
China Pharmacy
2026;37(16):2112-2118
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To investigate the effect and mechanism of Tangzhi formula（TZF） on improving glucose and lipid metabolism disorders in type 2 diabetes mellitus （T2DM） rats.METHODS Thirty SPF-grade SD rats were used to establish a T2DM rat model through high-fat diet feeding combined with intraperitoneal injection of streptozotocin. After successful modeling， the rats were divided into the model group， metformin group （positive control， 0.18 g/kg）， and TZF low-， medium-， and high-dose groups （5， 10， and 20 g/kg）， with 6 rats in each group. An additional 6 rats were selected as the blank group. The rats in each group were orally administered the corresponding volume of drug solution or saline， and continuous dosing was performed for 6 weeks， once daily. Fasting blood glucose （FBG）， area under the curve of oral glucose tolerance test （OGTT-AUC）， area under the curve of intraperitoneal insulin tolerance test （IPITT-AUC）， serum total cholesterol （TC）， triglyceride （TG）， low-density lipoprotein cholesterol （LDL-C）， and high-density lipoprotein cholesterol （HDL-C） levels were measured. Hematoxylin-eosin （HE） staining and oil red O staining were used to observe hepatic pathological morphology and lipid deposition. Differentially expressed proteins in liver tissues were screened by proteomics analysis， and key proteins in signaling pathways were verified by Western blot and immunofluorescence staining.RESULTS Compared with the blank group， the levels of FBG， OGTT-AUC， IPITT-AUC， LDL-C， TG， and TC in the model group were significantly increased （ P ＜0.05）， while HDL-C level was significantly decreased （ P ＜0.05）； the liver tissues showed disordered hepatic cords， punctate necrosis of hepatocytes， and significant lipid deposition， the NAFLD activity score and positive area of lipid droplets were significantly increased（ P ＜0.05）. Compared with the model group， the above indicators in TZF low-， medium-， and high-dose groups and metformin group were significantly reversed （ P ＜0.05）； hepatic pathological injury and lipid deposition were alleviated. Proteomics results showed that a total of 442 differentially expressed proteins were screened between the model group and the blank group， and 358 differentially expressed proteins were screened between the TZF high-dose group and the model group. Among these differentially expressed proteins， multiple proteins closely related to glucose and lipid metabolism showed a reversal trend after TZF intervention. Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis showed that the peroxisome proliferator-activated receptor （PPAR） signaling pathway was significantly enriched. The validation experiment results showed that TZF could significantly up-regulate the expression of PPARα， PPARγ， and apolipoprotein A1 （ApoA1） in rat liver tissues （ P ＜0.05）， and down-regulate the expression of stearoyl-CoA desaturase 1 （SCD1） and perilipin 2 （PLIN2） （ P ＜0.05）.CONCLUSIONS TZF can improve glucose and lipid metabolism disorders in T2DM rats； its mechanism may be related to the activation of the PPAR signaling pathway and the regulation of downstream lipid metabolism-related proteins SCD1， PLIN2， and ApoA1.
