硫化氢对幽门螺杆菌感染GES-I细胞CSE，NF-KB及lL-8mRNA表达的影响

目的：观察硫化氢（hydrogen sulfide，H2S）对幽门螺杆菌（Hpylori）感染的GES．1细胞CSE，NF—gB及IL．8mRNA表达及其形态学的影响，探讨其对Hpylori所致胃黏膜细胞炎症的作用及机制。方法：将GES．1细胞培养24hA分为对照组（不加Hpylori及NariS）、Hpylori组、NaHS组（又分为4个亚组，分别加入50，100，200或400umol／LNariS）和Hpylori＋NariS组（又分为4个亚组，分别加入Hpylori与50，100，200或400~tmol／LNariS），每组分别培养3，6，及12h，用RT-PCR法检测各组GES-1细胞CSE，NF-kB及IL-8mRNA表达，并分析其相关性。结果：Hpylori组CSE，NF—gB及IL-8mRNA表达均较对照组增加／1（P〈0．05），200umol／LNariS组和4008mol／LNariS组CSE表达较对照组降低（p〈o．05）；而NariS各组NF，KB和IL-8mRNA表达与对照组比较差异无统计学意义（P〉O．05）；NariS各组、Hpylori＋200um01／LNaHS组及Hpylori＋400umol／LNaris组CSE，NF—KB及IL-8m对弧表达均较Hpylori组降低（P〈0．05）；Hpylori组、Hpylori＋200umol／LNariS组及Hpylori＋4008mol／LNaHS组CSE，NF—KB及IL．8mRN．~达之间均呈正相关（P〈O．05）。结论：Hpylori诱导GES-1细胞NF．gB和IL-8mRNA表达，并上调CSEmRNA表达；200和400tmol／LNaHS能抑NH．pylori感染诱导的GES—1细胞NF．KB和IL-8mRN朦达，改善Hpylori感染所致的细胞形态学变化，对细胞起保护作用。

Effect of hydrogen sulfide on the expression of CSE,NF-kB,and IL-8 mRNA in GES-I cells with Helicobacterpylori infection

Objective： To investigate the effect of hydrogen sulfide （HzS） on the expression of CSE, NF-~cB, and IL-8 mRNA in GES- 1 cells with Helicobacter pylori （H. pylori） infection and to explore itsmechanism on gastric mucosa inflammation caused by H. pylori. Methods： GES-1 cells were cultured for 24 h and divided into a control group （neither H. pylori nor NariS）, an H. pylori group, a NariS group （which was further divided into 4 groups at 50, 100, 200, or 400 anol/L NariS）, and H. pylori ＋ NariS group （which was further divided into 4 groups at 50, 100, 200, or 400 arnol/L NariS）. Each group was then cultured for 3, 6, or 12 h. The expression of CSE, NF-kB, and IL-8 mRNA was measured by RT-PCR, and their correlation was analyzed. Results： The expression of CSE, NF-lcB, and IL-8 mRNA in GES-1 cells in the H. pylori group was higher than that in the control group. The expression of CSE in the 200 tmaol/L NariS group and 400 utmol/L NariS group was lower than that of the control group （P〈0.05）, whereas the expression of NF-~cB and IL-8 in all NariS groups had no statistical differences compared with the control group （P〉0.05）. qqae expression of CSE, NF-r,B, and IL-8 mRNA in all groups of NariS, H. pylori ＋ 200 utmol/L NariS group, and H. pylori ＋ 400 xrnol/L NariS group was lower than that in the H. pylori group （P〈0.05）. There was positive correlation among the expressions of CSE, NF-kB, and IL-8 mRNA in the H. pylori group, the H. pylori ＋ 200 utmol/L NariS group, and the H. pylori ＋ 400 uunol/L NariS group （P〈0.05）. Conclusion： H. pylori can induce NF-r,B and IL-8 mRNA expression and upregulate CSE mRNA expression. At 200 and 400 unol/L, NariS can suppress H. pylori-induced NF-KB and IL-8 mRNA expression and ameliorate the morphology of H. pylori-induced GES-1 iniur~ which may protect gastric epithelial cells by H. pylori infection.