Inhibitory effect of phillyrin on myocardial fibrosis in diabetes mellitus rats by activating PI3K/AKT/eNOS signaling pathway
10.3969/j.issn.1000-484X.2025.08.013
- VernacularTitle:连翘苷激活PI3K/AKT/eNOS信号通路对糖尿病大鼠心肌纤维化的抑制作用
- Author:
Xuan KE
1
;
Yuanheng ZHANG
1
;
Dongsheng LI
1
;
Long YAN
1
;
Bei WAN
1
Author Information
1. 武汉市第三医院心内科,武汉 430060
- Publication Type:Journal Article
- Keywords:
Phillyrin;
Diabetes mellitus;
Myocardial fibrosis;
Inositol 3-kinase/protein kinase B/endothelial nitric oxide;
Endo-thelial mesenchymal transdifferentiation
- From:
Chinese Journal of Immunology
2025;41(8):1873-1878
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To study the inhibitory effect of phillyrin(PN)on myocardial fibrosis in diabetes mellitus(DM)rats and its mechanism.Methods:Sixty SD rats were randomly assigned:control group,DM group,low-dose PN group(10 mg/kg),high-dose PN group(30 mg/kg)and LY294002 group(PN 30 mg/kg+PI3K inhibitor 100 mg/kg),with 12 rats in each group,DM model was constructed by streptozotocin.After 8 weeks of drug intervention,FBG was measured with a blood glucose meter,the LVFS,LVEF,LVPWT and E/A were measured by echocardiography;HE staining and Masson staining were used to changes of myocardium,and the CVF was measured;ELISA was used to detect the Vaspin,TNF-α,IL-1β and IL-6 in myocardium;Western blot was used to detect the expressions of α-SMA,FSP-1,CD31,COL1,PI3K,p-PI3K,AKT,p-AKT,eNOS and p-eNOS in myocardium.Results:Compared with the control group,the myocardial cells in DM group were swollen,gaps were enlarged,and collagen fibers were in-creased,the levels of FBG,CVF,Vaspin,TNF-α,IL-1β,IL-6,α-SMA,FSP-1 and COL1 were increased obviously,the levels of LVFS,LVEF,LVPWT,E/A,CD31,p-PI3K/PI3K,p-AKT/AKT,p-eNOS/eNOS were reduced obviously(P<0.05).Compared with the DM group,the swelling of myocardial cells,the normal gap,and the decrease of collagen fibers in the low-dose and high-dose PN groups were reduced,the levels of FBG,CVF,Vaspin,TNF-α,IL-1β,IL-6,α-SMA,FSP-1 and COL1 were decreased obviously,the LVFS,LVEF,LVPWT,E/A,CD31,levels of p-PI3K/PI3K,p-AKT/AKT,p-eNOS/eNOS were increased obviously(P<0.05).LY294002,AKT/eNOS pathway inhibitor,obviously weakened the relieving effect of PN on myocardial fibrosis in DM rats.Conclu-sion:PN may improve cardiac function,reduce myocardial fibrosis and inhibit endothelial mesenchymal transdifferentiation(EndMT)in DM rats by activating PI3K/AKT/eNOS pathway.
