Exploration of Mechanism of Gegen Qinliantang in Improving Skeletal Muscle Insulin Resistance Based on Transcriptomics
10.13422/j.cnki.syfjx.20250715
- VernacularTitle:基于转录组学探讨葛根芩连汤改善骨骼肌胰岛素抵抗机制
- Author:
Weinan LIU
1
;
Jiaxiang YU
1
;
Hanwen ZHANG
1
;
Jiayi JING
1
;
Jinning TONG
1
;
Wenshun ZHANG
2
;
Yi WU
2
Author Information
1. Liaoning University of Traditional Chinese Medicine（TCM）， Shenyang 110847， China
2. Liaoning Academy of TCM/The Second Affiliated Hospital of Liaoning University of TCM， Shenyang 110034， China
- Publication Type:Journal Article
- Keywords:
Gegen Qinliantang;
insulin resistance;
transcriptomics;
apoptosis;
mechanism;
improvement
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2026;32(4):29-40
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the mechanism by which Gegen Qinliantang（GQT） improves skeletal muscle insulin resistance. MethodsThe db/m mice were used as the normal group， while db/db mice were assigned to a model group， low-dose （3.12 g·kg-1）， medium-dose （6.24 g·kg-1）， and high-dose （12.48 g·kg-1） GQT groups， and a Western medicine group （semaglutide， 0.045 mg·kg-1），n=6 in each group. All groups received corresponding interventions. Intraperitoneal glucose tolerance test （IPGTT）， intraperitoneal insulin tolerance test （IPITT）， and hematoxylin-eosin （HE） staining were used to evaluate insulin resistance and therapeutic efficacy. Serum lipid levels were measured using an automatic biochemical analyzer， and apoptosis in skeletal muscle was assessed via TUNEL assay. Transcriptome sequencing combined with gene ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） analyses was performed to identify differentially expressed genes （DEGs）. Real-time quantitative polymerase chain reaction （Real-time PCR） was used to validate gene expression. Molecular docking was applied to evaluate the binding patterns between active components of GQT and key regulatory genes to elucidate pharmacological mechanisms. ResultsCompared with the model group， the medium-dose and high-dose GQT groups showed significantly reduced fasting blood glucose （FBG） levels （P<0.01）. Triglycerides （TG）， total cholesterol （TC）， and low-density lipoprotein cholesterol （LDL-C） were markedly decreased （P<0.01）， while high-density lipoprotein cholesterol （HDL-C） was significantly increased （P<0.01）. IPGTT， IPITT， and HE staining demonstrated that GQT enhanced insulin sensitivity and restored skeletal muscle morphology. GQT also alleviated apoptosis in skeletal muscle tissue. Transcriptome analysis revealed that GQT primarily affected biological processes such as oxidative phosphorylation， metabolic pathways， cellular processes， and protein binding. Real-time PCR results showed that CBR2， CDK6， F830016B08Rik， IL-1β， Rab27b， and COLEC12 were key regulatory genes. Molecular docking demonstrated that CBR2， IL-1β， Rab27b， and COLEC12 formed stable binding with the main active components of GQT. The therapeutic effects of high- and medium-dose GQT were comparable to those of the semaglutide group. ConclusionGQT improves skeletal muscle insulin resistance， potentially by regulating apoptosis as part of its underlying biological mechanism.
