关键词: 氧化应激, 骨骼肌卫星细胞, MAPK, p38, JNK

Abstract:

【Objective】 Mitogen-activated protein kinases (MAPKs) signaling pathway was investigated to screen which one plays a key role in broiler skeletal muscle satellite cells (SCs) under oxidative stress induced by dexamethasone (DEX) in vitro. 【Method】 The broilers skeletal muscle SCs were assigned into one of the ten treatments: control (I), DEX (Ⅱ), inhibitor p38 MAPK (Ⅲ), DEX plus inhibitor p38 MAPK (Ⅳ), inhibitor JNK (Ⅴ), DEX plus inhibitor JNK (Ⅵ), inhibitor ERK5 (Ⅶ), DEX plus inhibitor ERK5 (Ⅷ), inhibitor ERK1/2 (Ⅸ), DEX plus inhibitor ERK1/2 (Ⅹ). The treatments exclude treatments I and Ⅱ were treated with inhibitors for 30 min before treating with DEX and normal medium for 24 h. The relative production of malonaldehyde (MDA), reactive oxidative species (ROS), the activities of superoxide dismutase (SOD) and glutathione S-transferase (GST) were measured, respectively. Polymerase chain reaction (PCR) was employed to assess SOD and GST gene expression.【Result】 Compared with DEX, the MDA and ROS concentrations were decreased (P＜0.05) in all the inhibitors-treated groups. The concentration of MDA and ROS in treatment with inhibitors were higher than that in treatment with DEX (P＜0.05) The MDA and ROS concentrations of treatment with DEX plus inhibitor ERK5 and of treatment with DEX plus inhibitor ERK 1/2 were significantly higher than that of treatment with inhibitor ERK5 and treatment with inhibitor ERK1/2 (P＜0.05). However, there were no significant differences in MDA and ROS concentrations among treatment with DEX plus inhibitor p38 MAPK, treatment with DEX plus inhibitor JNK and treatment with inhibitor p38 MAPK, treatment with inhibitor JNK (P＞0.05). The activities of SOD and GST of all the inhibitors-treated groups were significantly higher than those of DEX group (P＜0.01). The activities of SOD and GST of treatment with DEX plus inhibitor ERK5 and treatment with DEX plus inhibitor ERK 1/2 were significantly lower than those of treatment with inhibitor ERK5 and treatment with inhibitor ERK1/2 (P＜0.01), while there were no significant differences in treatment with DEX plus inhibitor p38 MAPK, treatment with DEX plus inhibitor JNK and treatment with inhibitor p38 MAPK, and treatment with inhibitor JNK (P＞0.05). DEX could inhibit the expression of SOD and GST gene, the inhibition rate was more than 37%. On the contrary to ERK5 and ERK1/2 pathway, DEX treatment had no significant effects on the expression of SOD and GST gene while the p38 MAPK and JNK pathway were inhibited. 【Conclusion】 The p38 MAPK and JNK pathway play a key role in broiler breast muscle SCs under oxidative stress induced by DEX.

Key words: oxidative stress, breast muscle satellite cell, MAPK, p38, JNK