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Effects of lactobacillus on phosphorylated p38 mitogen-activated protein kinase and apoptosis in SGC-7901 cells treated with lipopolysaccharide of Helicobacter pylori
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- Author:
- No author available
- Journal Title:
- WORLD CHINESE JOURNAL OF DIGESTOLOGY
- Issue:
- 8
- DOI:
- 10.3969/j.issn.1009-3079.2007.08.003
- Key Word:
- 乳酸杆菌;幽门螺旋杆菌;脂多糖;SGC7901细胞;p38丝裂原活化蛋白激酶;细胞凋亡
Abstract： 目的:探讨保加利亚乳酸杆菌(lactobacillus bulgaricus,LBG)对幽门螺旋杆菌悉尼株脂多糖(H pyloriSS1-LPS)作用下SGC-7901细胞的p38有丝分裂原活化蛋白激酶(p38MAPK)磷酸化水平和凋亡率的影响.方法:使用LBG(1×1013CFU/L)或p38MAPK通路阻滞剂SB203580(10 μmol/L)预处理SGC-7901细胞,1 h后分别加入2.5×103,2.5×104,2.5×105EU/L的H pyloriSS1-LPS,干预2 h后使用免疫细胞化学方法检测各组细胞磷酸化p38MAPK(P-p38MAPK)的水平,4,5,6 h后使用MTT法检测细胞活性,6 h后使用流式细胞仪检测各组细胞凋亡率.结果:与对照组比较,H pyloriSS1-LPS直接干预后,SGC-7901细胞的活性明显下降(0.1 64±0.028 vs 0.622±0.068,P＜0.05),凋亡率(10.000%±0.510% vs 4.175%±0.206%,P＜0.05)和P-p38MAPK水平明显上升(79.771±1.424 vs 4.075±0.135,P＜0.01),呈剂量依赖性;LBG预处理各组的细胞凋亡率和P-p38MAPK水平无明显改变;SB203580预处理各组的细胞活性和细胞凋亡率无明显改变.结论:HpyloriSS1-LPS可诱导SGC-7901细胞凋亡,其机制可能包括诱导生成P-p38MAPK;而LBG能对抗H pyloriSS1-LPS的促凋亡作用,其机制可能抑制H pyloriSS1-LPS诱导生成P-p38MAPK.
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