Role of ROS/PKC/p38 MAPK pathway in protective effects of polysac-charide from Fructus corni on rat cardiomyocytes against hypoxia-reoxy-genation injury
10.3969/j.issn.1000-4718.2014.12.015
- VernacularTitle:ROS／PKC／p38MAPK途径在山茱萸多糖抑制心肌细胞缺氧／复氧损伤的作用
- Author:
Lina LAI
;
Lihua SONG
;
Xiaojing ZHANG
;
Xiaoyi ZHANG
;
Jingwen LEI
;
Fang LIU
;
Chunhua GUO
;
Xiaoliang SONG
- Publication Type:Journal Article
- Keywords:
Fructus corni;
Polysaccharide;
Hypoxia/reoxygenation;
Cardiomyocytes;
Reactive oxygen species
- From:
Chinese Journal of Pathophysiology
2014;(12):2201-2205
- CountryChina
- Language:Chinese
-
Abstract:
[ ABSTRACT] AIM:To investigate the effect of polysaccharide from Fructus corni ( PFC) on cardiomyocytes against hypoxia/reoxygenation ( H/R) injury and its possible relationship with ROS/PKC/p38 MAPK pathway.METHODS:Prima-ry cardiomyocytes were isolated from neonatal SD rats and randomly divided into normal group, H/R group, PFC (20 mg/L, 100 mg/L and 200 mg/L) preconditioning+H/R groups, chelerythrine+PFC (100 mg/L)+H/R group and SB203580+PFC (100 mg/L)+H/R group.The cell viability was measured by inverted microscopic observation.Apoptosis in the car-diomyocytes was detected by Hoechst 33258 staining and fluorescence microscopy.The levels of lactate dehydrogenase ( LDH) and superoxide dismutase ( SOD) in the cell culture supernatants, and the reactive oxygen species ( ROS) in the cells were also measured by microplate reader.The protein levels of PKC, p-p38 MAPK and HSP70 in the cells were detec-ted by Western blotting.RESULTS:Compared with normal group, the cell viability and beating frequency were decreased in H/R group.LDH and ROS contents, apoptotic rate and p-p38 MAPK level increased significantly (P<0.01).Compared with H/R group, PFC preconditioning increased beating frequency, SOD activity and the protein level of PKC and HSP70, and decreased ROS production, the protein level of p-p38 MAPK and cell apoptotic rate.However, the effect of PFC was in-hibited by chelerythrine or SB203580.CONCLUSION:PFC may protect cardiomyocytes from hypoxia/reoxygenation injury. Its mechanism is possibly involved in the inhibition of ROS via increasing the activity of SOD and the activation of PKC, and suppression of excessive activation of p38 MAPK.
