Mechanism of inhibitory effect of catalpol on TNF-α induced HAECs cell damage.
10.19540/j.cnki.cjcmm.20181109.001
- Author:
Can-Yao XU
1
;
Yu-Kun ZHANG
2
;
Hui-Jun SUN
2
;
Hong ZHANG
1
Author Information
1. the Second Affiliated Hospital of Dalian Medical University Dalian 116023,China.
2. College of Pharmacy,Dalian Medical University Dalian 116044,China.
- Publication Type:Journal Article
- Keywords:
AMPK;
TNF-α;
autophagy;
catalpol;
oxidative stress
- MeSH:
Humans;
Iridoid Glucosides;
pharmacology;
Iridoids;
Oxidative Stress;
Reactive Oxygen Species;
Tumor Necrosis Factor-alpha
- From:
China Journal of Chinese Materia Medica
2019;44(4):796-802
- CountryChina
- Language:Chinese
-
Abstract:
Catalpol is an iridoid glycoside extracted from the root of Rehmannia glutinosa. It has been reported to have antioxidant stress effects. Adenosine 5' monophosphate-activated protein kinase( AMPK) plays an important role in inhibiting oxidative stress. This study was designed to investigate the protective effects of catalpol on TNF-α-exposed human aorta epithelial cells( HAECs) via inhibit oxidative stress,and the relationship between catalpol and AMPK was detected by RNA interference technique. Levels of superoxide dismutase( SOD),malonaldehyde( MDA),glutathione( GSH) and lactate dehydrogenase( LDH) were measured with a colorimetric assay kit. The level of ROS was measured with FACS calibur. Western blot was employed to detect the protein expression of AMPK,phosphorylated-AMPK and NOX4. Finally,RNA interference technique was used to investigate the role of AMPK in catalpol-induced protective effects. TNF-α treatment decreased the expression of phosphorylated-AMPK protein level,however,catalpol could reverse the decreased phosphorylated-AMPK level. Catalpol could inhibit NOX4 protein expression and decrease ROS overproduction. After using AMPK siRNA that effects of catalpol on ROS overproduction and NOX4 protein expression inhibition were attenuated. The above results suggest that catalpol inhibits oxidative stress in TNF-α-exposed HAECs by activating AMPK.
