乳酸杆菌对幽门螺旋杆菌脂多糖作用下的SGC-7901细胞p38MAPK磷酸化水平和凋亡率的影响  

Effects of lactobacillus on phosphorylated p38 mitogen-activated protein kinase and apoptosis in SGC-7901 cells treated with lipopolysaccharide of Helicobacter pylori

作　　者：周超[1] 马洪升[1] 

机构地区：[1]四川大学华西医院消化内科,四川省成都市610041

出　　处：《世界华人消化杂志》2007年第8期807-812,共6页World Chinese Journal of Digestology

基　　金：四川省科技厅应用基础研究项目;No.04JY029-090-1

摘　　要：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(1×1013 CFU／L)或p38MAPK通路阻滞剂SB203580(10μmol／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(0．164±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 pylotiSS1-LPS的促凋亡作用,其机制可能抑制H pyloriSS1-LPS诱导生成P-p38MAPK．AIM： To investigate effects of lactobacillus bulgaricus （LBG） on the levels of phosphorylated p38 mitogen-activated protein kinase （P-p38MAPK） and apoptosis index （AI） in gastric cancer cell line SGC-7901 treated with lipopolysaccharide of H pylori Sydney strain 1 （H pyloriSS1-LPS）. METHODS： Human gastric cancer cell line SGC-7901 was treated with H pyloriSS1-LPS at the concentration of 2.5×10^3, 2.5×10^4, 2.5×10^5 EU/L, respectively, after pretreatment for 1 hour with 10 μmol/L SB203580 （blocker of p38MAPK） or 1×10^13 CFU/L LBG. The level of P-p38MAPK was analyzed by immunocytochemistry after 2 hours of H pyloriSS1-LPS treatment. The cell activity was detected by MTr assay after 4, 5 and 6 hours of treatment, and the apoptosis was measured by flow cytometry at the 6^th hour. RESULTS： H pyloriSS1-LPS inhibited cell activity （0.164 ± 0.028 vs 0.622 ± 0.068, P 〈 0.05） and up-regulated the level of P-p38MAPK （79.771 ± 1.424 vs 4.075 ± 0. 135, P 〈 0.01） and AI value （10.000% ± 0.510% vs 4.175% ± 0.206%, P 〈 0.05） in a dose-dependent manner. The level of P-p38MAPK and AI value in SGC-7901 cells were not significantly different between LBG pretreatment group and the controls, and the cell activity and AI value were not markedly different between SB203580 pretreatment group and the controls. CONCLUSION： H pyloriSS1-LPS may induce the apoptosis of SGC-7901 cells by activating the phosphorylation of p38MAPK, while LBG can prevent H pyloriSS1-LPS-induced apoptosis of SGC-7901 cells by inhibiting the phosphorylation of p38MAPK.

关 键 词：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 

分 类 号：R573[医药卫生—消化系统]