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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.
OBJECTIVE: To investigate the signal transduction pathway of p38MAPK in the function of Bip protein-mediated mild hypothermia in rat macrophages.Methods: The rat macrophages were pretreated with p38MAPK inhibitor and the cells were placed in a 41 ℃ incubator (Control group) and macrophages (stress group) at 60 min after heat shock of 41 ℃ for 1h, respectively The phagocytosis, killing and chemotaxis function of macrophages in 3 groups were detected, and the expressions of p38MAPK protein and Bip protein were also detected.Results: Compared with the stress group, the p38MAPK inhibitor pretreated the macrophages in the spleen, Macrophages phagocytosis, chemotactic and cytotoxic activity was significantly reduced (0.17 ± 0.01 vs0.74 ± 0.03,33.32 ± 3.55vs82.07 ± 5.17,24.20% ± 2.39% vs60.80% ± 4.02%, both P <0.01); The expression of p38MAPK protein in stress group was significantly up-regulated. After pretreatment with p38MAPK inhibitor, the expression of p38MAPK protein was inhibited in p38MAPK inhibitor group (p38 / β-actin: 2.863 ± 0.794 vs4.752 ± 1.386, P <0.01). The expression of Bip protein (Bip / β-actin) was also decreased from 1.270 ± 0.535 in the stress group to 1.028 ± 1.0 in the inhibition group by pretreatment with p38MAPK inhibitor 61 (P <0.05) .Conclusion: p38MAPK inhibitor can significantly inhibit macrophage phagocytosis, chemotaxis and cytotoxicity, as well as p38MAPK and Bip protein expression in mild heat stress rats.