Effects of cistanche phenylethanol glycosides on the cardiac hypertrophy and PI3K/PKB signaling pathway in rats with pressure overload
10.3969/j.issn.1001-1978.2020.04.024
- Author:
Qiong-Ling FAN
1
Author Information
1. College of Nursing, Xinjiang Medical University
- Publication Type:Journal Article
- Keywords:
Abdominal aorta coarctation;
Cardiac hypertrophy;
Cistanche Phenylethanol Glycosides;
Phosphorylated;
PI3K/PKB;
Pressure overload
- From:
Chinese Pharmacological Bulletin
2020;36(4):583-588
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the inhibitory effect of cistanche phenylethanol glycosides (CPhGs) on cardiac hypertrophy in rats caused by pressure overload and its related mechanism. Methods Male SD rats(n =70) were randomly divided into control group (Con), sham operation group (Sham), model group (Mod), positive control group (Vst), and different CPhGs dosage (125, 250, 500 mg • kg-1) groups. Cardiac ultrasound indexes, heart-weight to body-weight index (HWI), cardiac histopathological changes, and the area of myocardical cells (AMC) were detected. Plasma ET-1 and BNP levels were detected by Elisa, and protein expressions of phosphorylated PI3K(p-PI3K), PI3K, phosphorylated PKB (p-pKB) and PKB were detected by Western blot. Results Compared with Mod group, LVPWT, HWI, plasma ET-1, BNP and AMC decreased to different degrees. LVEDD, LVEF, LVFS, the protein expressions of myocardial tissues pPI3K and p-PKB increased to different degrees in CPhGs groups. Moreover, the indexes of CPhGs 250 and 500 mg • kg-1 groups were significantly improved compared to those of Mod group (P < 0. 05 or 0. 01). Compared with Vst group, there were no significant difference in CPhGs 500 mg • kg-1 group. Conclusions CPhGs could inhibit cardiac hypertrophy in rats induced by pressure overload, which might be related to the activation of PI3K/PKB signaling pathway.
