长链非编码RNA MIAT在幽门螺杆菌感染胃溃疡中的表达和作用机制

Expression and mechanism of lncRNA MIATin gastric ulcer infected with Helicobacter pylori

目的探讨长链非编码RNA MIAT在幽门螺杆菌感染的胃溃疡中的表达意义和作用机制。方法选取120例幽门螺杆菌感染的胃溃疡患者及100例经胃镜检查胃黏膜正常的患者,检测胃溃疡和正常胃黏膜组织以及血浆中MIAT的表达。构建幽门螺杆菌感染的人胃黏膜上皮细胞GES-1损伤模型,观察MIAT过表达后,幽门螺杆菌感染的胃黏膜细胞增殖、凋亡和炎症因子变化。结果胃溃疡组溃疡组织和血浆的MIAT表达水平均低于正常组,幽门螺杆菌阳性的胃溃疡患者的溃疡组织和血浆中的MIAT表达水平均低于幽门螺杆菌阴性的胃溃疡患者,差异均有统计学意义(P<0.001)。幽门螺杆菌感染后GES-1细胞的MIAT表达水平降低,差异有统计学意义(P<0.001)。与未转染MIAT的GES-1细胞和未转染MIAT的HP感染的GES-1细胞比较,转染MIAT后,HP感染的GES-1细胞的增殖增加,凋亡率和炎症因子IL-1β、IL-6及TNF-α水平均降低,差异有统计学意义(P<0.05)。结论长链非编码RNA MIAT在幽门螺杆菌感染的胃溃疡中存在低表达现象,MIAT的过表达可促进幽门螺杆菌感染后的胃黏膜上皮细胞增殖,降低凋亡率和炎症反应。

Objective To investigate the expression and mechanism of lncRNA MIAT in gastric ulcer infected with Helicobacter pylori.Methods A total of 120 patients with gastric ulcer infected with Helicobacter pylori and 100 patients with normal gastric mucosa were collected.The expression of MIAT in gastric ulcer and normal gastric mucosa tissues and plasma were detected.Gastric mucosal cell injury model was established using GES-1 infected Helicobacter pylori.The proliferation,apoptosis and inflammation of gastric mucosal cells were detected after MIAT overexpression.Results The expression of MIAT in ulcer tissue and plasma of patients with gastric ulcers was lower than that in normal group(P<0.001).The expression of MIAT in ulcer tissue and plasma of patients with Helicobacter pylori infection was also lower than that of the negative group(P<0.001).The expression of MIAT in GES-1 cells was decreased after Helicobacter pylori infection(P<0.001).Compared with GES-1 cells without MIAT transfection and GES-1 cells infected by Helicobacter pylori without MIAT transfection,Helicobacter pylori-infected GES-1 cells showed increased proliferation,and the apoptosis rate and the levels of IL-1β,IL-6 and TNF-αwere decreased(P<0.05).Conclusions lncRNA MIAT has a low expression in gastric ulcers infected with Helicobacter pylori.Overexpression of MIAT promotes proliferation of gastric mucosal epithelial cells after Helicobacter pylori infection and reduces apoptosis and inflammatory response.