和胃宝通过COX-2通路减轻氧化应激防治小鼠实验性胃溃疡的机制研究

Heweibao Alleviates Oxidative Stress in Mice with Experimental Gastric Ulcer through Cyclooxygenase-2 Pathway

目的:探讨和胃宝对实验性胃溃疡氧化应激反应的作用及其调节机制。方法:雄性BARB/c小鼠随机分为空白对照组、模型组、和胃宝高、中、低剂量组和法莫替丁组。幽门螺旋杆菌(Helicobacter pylori,Hp)合并乙酸诱导胃溃疡,观察和胃宝对乙酸诱导小鼠胃溃疡的病理改变,化学法测定胃溃疡组织匀浆液中SOD/MDA的含量,免疫组化和Western blot分别检测胃溃疡组织中环氧合酶-2(cyclooxygenase 2,COX-2)和诱导型一氧化氮合酶(induced nitric oxide synthase,iNOS)的表达。结果:和胃宝组高、中剂量组改善组织病理结构并显著提高SOD活力(P<0.01,P<0.05),降低Hp抗体表达水平(P<0.01,P<0.05),高剂量组显著降低MDA的含量(P<0.05),免疫组化、Western blot结果显示,模型组COX-2、iNOS表达明显升高(P<0.05)。和胃宝高、中剂量组显著降低COX-2表达;法莫替丁降低COX-2表达(P<0.01),对iNOS表达的影响差异无统计学意义。结论:和胃宝高、中剂量组显著减轻实验性胃溃疡,可能与其通过抑制COX-2通路减轻氧化应激水平有关。

Objective： To investigate the effects of Heweibao （HWB） on mice with experimental ulcer and its regulatory mechanism. Methods： Sixty male BARB/c rats weighed 22 - 24 g were divided into six groups ： control group, model group, high dose HWB, middle dose HWB, low dose HWB and famotidine group. Helicobacter pylori （Hp） combined with acetic acid were used to induce gastric ulcer. Pathological, Chemical colorimetric, immunohistochemical method and Western Blotting are performed to detect the gastric mueosal injury, MDA/SOD level and COX-2, induced nitric oxide synthase （iNOS） expression. Results： HWB significantly alleviates the gastric mucosa injury. HWB high dose and middle dose increase the SOD levels and decreases the Hp antibody level, high dose decreases the MDA contents. HWB high dose and middle dose decrease the expression of COX-2. Famotidine lowers the expression of COX-2 but has no significant effect on iNOS. Conclusions： HWB can alleviate gastric ulcer induced by Hp ＆ acetic acid. The anti-ulceric effects of HWB are conferred by reducing oxidative stress manifested as decreased MDA and increased SOD through down- regulating COX-2 .