CAJ | 학술논문

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,1 h后恢复到37℃(抑制组),以未应激(对照组)和41℃热应激1 h后60 min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±0.01 vs 0.74±0.03,33.32±3.55 vs 82.07±5.17,24.20%±2.39% vs 60.80%±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p38 MAPK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±0.794 vs 4.752±1.386,P<0.01);Bip蛋白的表达(Bip/β-act in)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.
목적: 탐토p38MAPK재Bip단백개도적체외경도열응격대서거서세포공능개변중적신호작용.방법: p38MAPK억제제예처리대서비장거서세포,장세포치우41℃항온상중,사세포경도열응격,1 h후회복도37℃(억제조),이미응격(대조조)화41℃열응격1 h후60 min거서세포(응격조)위대조,분별검측3조거서세포탄서、살상、추화공능,동시검측p38MAPK단백화Bip단백적표체.결과: p38MAPK억제제예처리대서비장거서세포,여응격조비교,경도열응격후거서세포탄서、추화화살상활성명현강저(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%,균P<0.01);응격조p38MAPK단백표체명현상조,p38MAPK억제제예처리후,억제조p38 MAPK단백표체수도억제,여응격조비교차이유현저성(p38/β-actin: 2.863±0.794 vs 4.752±1.386,P<0.01);Bip단백적표체(Bip/β-act in)야인p38MAPK억제제예처리이유응격조적1.270±0.535강지억제조적1.028±1.061( P<0.05).결론: p38MAPK억제제가현저억제경도열응격대서거서세포탄서、추화화살상공능이급p38MAPK화Bip단백적표체.
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 ± 3.55vs 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 ± 0.5345dropped 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.