Canagliflozin attenuates hypertension induced myocardial hypertrophy and fibrosis via RAS and TGF-ß1/Smad pathway.

Autor: Ai-Hua Li, Qing-Qing Wang, Ying-Chun Qin, Yi-Lin Xie, Zhi-Qiang Yan
Předmět:
Zdroj: Journal of Hainan Medical University; Jul2022, Vol. 28 Issue 13, p6-15, 10p
Abstrakt: Objective: To investigate the effects of cagliazin, a sodium-glucose cotransporter 2 inhibitor (SGLT-2I), on ventricular remodeling in spontaneously hypertensive rats (SHR) through renin angiotensin system (RAS) and transforming growth factor -ß1(TGF-ß1). Methods: The experiment was divided into 4 groups: normal blood pressure control group, SHR group, cagliet net low-dose group (30mg/kg), cagliet net high-dose group (60mg/kg), once a day for 8 weeks. Normal blood pressure rats (WKY) were used as the control group to measure blood pressure with tail sleeve sphygmomanometer (BP) and blood glucose level was measured with glucose meter Cardiac function was evaluated by echocardiography, cell area of left ventricle was evaluated by histomorphology, real-time quantitative polymerase chain reaction and protein imprinting hybridization were used to detect TGF-ß1 Smad4 renin from type I collagen (Col1a) type III collagen (Col3a) matrix metalloproteinase 2(MMP-2) Expression results of angiotensin II1 type receptor 1(AGTR1) and Angiotensin II2 type receptor 2 (AGTR2). Results:After 8 weeks of administration, the cardiac weight/body weight ratio (HW/BW) of left ventricular weight/heart weight ratio (LVW/HW) of kaglinet low-dose group and high-dose group was statistically significant compared with that of spontaneous hypertensive rats (P
Databáze: Complementary Index