Hypoglycemic Mechanism of Gegen Qinliantang： An Exploration Based on GPR119/cAMP/GLP-1 Pathway
10.13422/j.cnki.syfjx.20220207
- VernacularTitle:基于GPR119/cAMP/GLP-1通路探讨葛根芩连汤的降糖机制
- Author:
Jun CHEN
1
;
Zi-xing QIAN
2
;
Meng-yang ZHU
2
;
Xiao LIN
2
;
Ya-mei GE
2
Author Information
1. Hubei Provincial Hospital of Traditional Chinese Medicine，Wuhan 430061，China
2. Hubei University of Chinese Medicine，Wuhan 430061，China
- Publication Type:Journal Article
- Keywords:
Gegen Qinliantang （GGQL）;
intestinal epithelial cells;
cyclic adenosine monophosphate （cAMP）;
glucagon-like peptide-1 （GLP-1）;
G protein-coupled receptor 119 （GPR119）;
type 2 diabetes mellitus
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2022;28(3):25-30
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo explore the effects of Gegen Qinliantang（GGQL） on the proliferation and apoptosis of intestinal epithelial cells as well as on the expression of cyclic adenosine monophosphate （cAMP）， G protein-coupled receptor 119 （GPR119）， and glucagon-like peptide-1 （GLP-1）， so as to explore its potential hypoglycemic mechanism. MethodTwenty-five Wistar rats were gavaged with GGQL at the dose of 23 g·kg-1 crude drug， twice a day， which meant that 6 mL was administered into each rat per day for preparing the GGQL-containing serum. After seven consecutive times of administration， the intestinal epithelial L （NCI-H716） cells were cultured with different concentrations （1%， 2.5%， 5%， 7.5%， and 10%） of GGQL. The cell proliferation was evaluated using cell counting kit-8 （CCK-8） and the apoptosis by flow cytometry. The GLP-1 and cAMP contents in cell supernatant were determined by enzyme-linked immunosorbent assay （ELISA）. The mRNA and protein GLP-1 and GPR119 levels were assayed by real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） and Western blot， respectively. ResultCompared with the control group， GGQL significantly reduced the proliferation of NCI-H716 cells（P<0.05）. As the GGQL concentration increased， its inhibitory effect became more obvious. GGQL at each concentration significantly promoted the apoptosis of NCI-H716 cells （P<0.05）. Compared with the control group， GGQL significantly up-regulated the expression of cAMP， GLP-1， and GPR119 （P<0.05）. The results showed that the effect of GGQL was positively correlated with its concentration， and 10% GGQL exhibited the best effect. ConclusionGGQL effectively inhibits the proliferation of NCI-H716 cells and promotes their apoptosis， and it may promote the secretion of GLP-1 by up-regulating the expression of cAMP and GPR119.
