Effect of catalpol on " glucose deprivation" cardiomyocyte injury based on estrogen receptor
10.3969/j.issn.1001-1978.2019.06.011
- Author:
Su-Yun WANG
1
Author Information
1. School of Pharmacy, Nanjing University of Chinese Medicine
- Publication Type:Journal Article
- Keywords:
Autophagy;
Catalpol;
Glucose deprivation;
Oxidative damage;
Rat cardiomyocytes;
ROS
- From:
Chinese Pharmacological Bulletin
2019;35(6):786-792
- CountryChina
- Language:Chinese
-
Abstract:
Aim: To investigate the effect of catalpol-mediated autophagy on oxidative damage of cardiomyocytes induced by glucose deprivation based on estrogen receptor(ER) and the related mechanism. Methods: The cardiomyocytes (H9c2) injury model in rat was induced by glucose deprivation for 6 h. The protective effect of catalpol on H9c2 injury and its mechanism were observed. The cells were divided into five groups: control group, model group, catalpol group (0. 28, 2. 8, 28 μmol · L-1). The effects of catalpol on reactive oxygen species (ROS), malondialdehyde (MDA) and superoxide dismutase (SOD) in cells were detected, and the effect of catalpol on autophagy was assessed by electron microscopy. ER blockers was used to detect whether the protective effect of catalpol on oxidative damage was related to ER. Lentivirus transfection was used to lower the expression of ER alpha, and the oxidative damage and autophagy of H9c2 treated with catapol or not were observed. Results: Compared with control group, the levels of ROS and MDA increased and SOD decreased in model group, and there was no significant difference in the expression of autophagy related proteins. Compared with model group, catalpol could reduce oxidative damage and increase autophagy level. After transfection of ER alpha with lentivirus, catalpol inhibited the level of oxidative damage and promoted the effect of autophagy compared with the empty virus catalpol group. Conclusions: Catalpol can activate autophagy by up-regulating the expression of ER alpha and inhibiting the oxidative damage of cardiomyocytes.
