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目的评估幽门螺杆菌(Hp)急、慢性感染对小鼠胃黏膜环氧合酶(COX)表达的影响。方法清洁级BALB／C小鼠共40只,分为阴性对照组(10只)予0．4 ml生理盐水灌喂,急性感染组(10只)予 0．4 ml Hp菌液灌喂,共5 d,该两组小鼠在最后一次灌喂后2周处死;另20只小鼠予0．4 ml Hp菌液灌喂,共5 d,在最后一次灌喂2个月后将小鼠均分为两组,治疗组予克拉霉素按每天13．5 mg／kg分2次灌喂,连续7 d(本组有1只小鼠死亡);慢性感染组予生理盐水,1个月后分别处死两组动物。取胃黏膜标本, 用免疫组化半定量法测定上述各组胃窦黏膜COX-1及COX-2的蛋白表达。结果四组小鼠胃黏膜小凹上皮均可见COX-1蛋白表达,各组阳性率差异无统计学意义(P>0．05)。与阴性对照组相比,急、慢性感染组COX-2蛋白表达均明显增加,其中慢性感染组治疗前COX-2阳性率明显高于急性感染组。慢性感染组治疗后阳性率与治疗前相比有所下降,但差异无统计学意义(P>0．05)。结论 Hp感染导致胃黏膜COX-2表达增加,对COX-1表达无明显作用,清除Hp后COX-2表达仍高于正常。
Objective To evaluate the effect of Helicobacter pylori (Hp) acute and chronic infection on gastric mucosal cyclooxygenase (COX) expression in mice. Methods A total of 40 clean BALB / C mice were divided into four groups: control group (n = 10), saline group (n = 10), saline group 5 d, the two groups of mice were sacrificed 2 weeks after the last feeding; the other 20 mice were fed with 0.4 ml of Hp solution for 5 days. After the last feeding for 2 months, the mice The patients in the treatment group were given clarithromycin at the dosage of 13.5 mg / kg every day for 2 days for 7 consecutive days (one died in this group). The rats in the chronic infection group were given normal saline for one month After the two groups of animals were executed. Gastric mucosa specimens were taken and the protein expressions of COX-1 and COX-2 in antral mucosa of the above groups were determined by semi-quantitative immunohistochemical method. Results The expression of COX-1 protein in gastric mucosa was observed in all four groups. The positive rate of COX-1 in each group was not significantly different (P> 0.05). Compared with the negative control group, COX-2 protein expression was significantly increased in acute and chronic infection group, in which the positive rate of COX-2 in chronic infection group was significantly higher than that in acute infection group. The positive rate of chronic infection group after treatment decreased compared with before treatment, but the difference was not statistically significant (P> 0.05). Conclusions Hp infection leads to the increase of COX-2 expression in gastric mucosa, but has no effect on the expression of COX-1. The expression of COX-2 is still higher than normal after Hp clearance.