p38MAPK对轻度热应激大鼠脾脏巨噬细胞免疫功能的影响  

Effect of p38MAPK on immunofunction of spleen macrophages from heat stressed rats

作　　者：黄长文[1] 蔡成行[1] 李光明[1] Aqeel Ahmed 李惠珍[1] 傅华群[1] 

机构地区：[1]南昌大学第二附属医院肝胆外科,江西省南昌市330006

出　　处：《世界华人消化杂志》2009年第17期1720-1725,共6页World Chinese Journal of Digestology

基　　金：江西省教育厅科技基金资助项目;No.2007094~~

摘　　要：目的:探讨p38MAPK在Bip蛋白介导的体外轻度热应激大鼠巨噬细胞功能改变中的信号作用.方法:p38MAPK抑制剂预处理大鼠脾脏巨噬细胞,将细胞置于41℃恒温箱中,使细胞轻度热应激,1h后恢复到37℃(抑制组),以未应激(对照组)和41℃热应激1h后60min巨噬细胞(应激组)为对照,分别检测3组巨噬细胞吞噬、杀伤、趋化功能,同时检测p38MAPK蛋白和Bip蛋白的表达.结果:p38MAPK抑制剂预处理大鼠脾脏巨噬细胞,与应激组比较,轻度热应激后巨噬细胞吞噬、趋化和杀伤活性明显降低(0.17±0.01vs0.74±0.03,33.32±3.55vs82.07±5.17,24.20%±2.39%vs60.80%±4.02%,均P<0.01);应激组p38MAPK蛋白表达明显上调,p38MAPK抑制剂预处理后,抑制组p38MAPK蛋白表达受到抑制,与应激组比较差异有显著性(p38/β-actin:2.863±0.794vs4.752±1.386,P<0.01);Bip蛋白的表达(Bip/β-actin)也因p38MAPK抑制剂预处理而由应激组的1.270±0.535降至抑制组的1.028±1.061(P<0.05).结论:p38MAPK抑制剂可显著抑制轻度热应激大鼠巨噬细胞吞噬、趋化和杀伤功能以及p38MAPK和Bip蛋白的表达.AIM： To investigate the role of p38MAPK in Bip protein-mediated functional changes of mild heat stressed rat splenic macrophages in vitro.METHODS： Rat splenic macrophages were pretreated with p38MAPK inhibitor and placed into 41℃ incubator for mild heat stress. One hour later, temperature was restored to 37℃ in inhibition group. Non stressed rat spleen macrophages were assigned to the control group, and macrophages which was heat stressed at 41℃ for 1 h （stress group） were used as controls, too. Three groups were detected for macrophage phagocytosis, cytotoxicity and chemotaxis. At the same time p38MAPK protein and Bip protein expressions were detected. RESULTS： p38MAPK inhibitor pretreated rat splenic macrophages, when compared with the stress group, their phagocytosis, cytotoxicity and chemotaxis were significantly lowered after mild heat stress （0.17 ± 0.01 vs 0.74 ± 0.03, 33.32 ± 3.55 vs 82.07 ± 5.17, 24.20% ± 2.39% vs 60.80% ± 4.02%, all P 〈 0.01）. In stress group p38MAPK protein expressions were significantly increased; compared with the stress group, p38MAPK protein expressions were significantly inhibited after p38MAPK inhibitor pretreatment in inhibition group （p38/β-actin： 2.863 ± 0.794 vs 4.752 ± 1.386, P 〈 0.01）. p38MAPK inhibitor pretreatment also caused changes in Bip protein expressions （Bip/β-actin） in the stress group from 1.2702 ± 0.5345 dropped to 1.0281 ± 1.0614 in inhibition group （P 〈 0.05）. CONCLUSION： p38 inhibitors can significantly inhibit mild heat stressed rat splenic macrophage phagocytosis, cytotoxicity and chemotaxis, which inhibit p38MAPK and Bip protein expressions.

关 键 词：轻度热应激 巨噬细胞 免疫 BIP 丝裂原激活的蛋白激酶 

分 类 号：R392.3[医药卫生—免疫学]