摘要
目的:了解低浓度N-甲基-N’-硝基-N-亚硝基胍(MNNG)对P38 MAPK的影响,以及谷胱甘肽(GSH)在该信号通路中的调节作用。方法:用L-丁硫氨酸-S,R-磺基(L-buthionine-S,R-sulfoximine)减少细胞谷胱甘肽含量后,采用Western印迹法比较MNNG处理组和对照组P38MAPK磷酸化状态,观察MNNG对P38磷酸化状态的影响。用光密度扫描仪测定各蛋白质条带吸光值。“P”为磷酸化P38MAPK的吸收值,“T”为总P38MAPK吸收值。在各时点以对照组磷酸化率P/T为1·0,计算MNNG组的相对磷酸化率。结果:BSO预处理24h后,MNNG处理2·5h的相对磷酸化率为0·84,2·5h处理后换DMEM全培养基3h的相对磷酸化率2·19。结论:细胞内GSH含量降低可促进P38MAPK的活性。
AIM： To explore the effect of low concentration of N - methyl - N - nitro - N - nitroguanidine （MNNG） on p38MAPK, and the function of glutathiolle （GSH） on p38MAPK. METHODS： Western blotting was applied to detect the p38MAPK phosphorylation in MNNG treatment group and control group. To study the effect of GSH on MNNG - regulated p38MAPK activity, the intracellular GSH level was reduced by pretreatment of L - buthionine - S, R - sulfoximine （ BSO）. Assuming the absorbance of band in control group as 1.0, the relative P/r values of the treatment groups were calculated, with the “P” served as absorbance values of phospho - p38MAPK and the “T” as absorbance values of total p38MAPK. RESULTS： In BSO pretreated groups,the relative P/T in samples treated with MNNG for 2.5 h was 0.84, and became 2.19 with 3 h more incubation in the fresh medium. CONCLUSION： GSH deletion increases the activity of p38MAPK in MNNG treatment.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2005年第8期1495-1497,共3页
Chinese Journal of Pathophysiology
基金
浙江省医药卫生重点课题(No.2D0008)
浙江大学中青年科研启动基金资助项目(No.419100-542906)
浙江省自然科学基金资助项目(No.29801)
浙江省教育厅课题(2003-0305)
