头花蓼对幽门螺杆菌胃炎大鼠血清干扰素-γ和白细胞介素-4含量的影响

Effects of Polygonum capitatum on Content of IFN-γ and IL-4 in Rats with Helicobacter pyloric Gastritis

目的:探讨苗药头花蓼对幽门螺杆菌(H.pylori)感染相关性胃炎大鼠血清干扰素-γ(IFN-γ)、白细胞介素-4(IL-4)含量的影响。方法:30只SD大鼠随机分为空白组、模型组及头花蓼组,采用H.pylori灌胃造模,空白组灌胃无菌脑心浸液肉汤,模型组和头花蓼组用消炎痛预处理后灌胃H.pylori制作H.pylori感染相关性胃炎大鼠模型,之后空白组和模型组大鼠灌胃生理盐水、头花蓼组大鼠灌胃头花蓼2周;采用HE染色评估胃黏膜炎炎症损伤程度,酶联免疫(ELISA)法检测3组大鼠血清IFN-γ、IL-4含量,实时荧光定量PCR(real time-PCR)检测胃黏膜中IFN-γ、IL-4 mRNA的相对表达水平。结果:H.pylori灌胃造模后,大鼠胃窦黏膜有H.pylori定植,HE染色结果显示模型组大鼠胃组织呈现相关性胃炎病理形态改变;头花蓼干预后,H.pylori感染大鼠胃黏膜炎症明显改善,IFN-γmRNA表达水平明显下调、IFN-γ血清含量明显降低,与模型组比较差异均有统计学意义(P<0.05);而头花蓼干预对IL-4分泌的影响比较轻。结论:头花蓼可减轻H.pylori对胃黏膜炎性损伤,其机制可能是通过下调IFN-γmRNA转录水平而实现的。

Objective ： To investigate the effects of Polygonum capitatum on content of IFN-γ and IL- 4 in rats with Helicobacter Pyloric gastritis. Methods： 30 SD rats were randomly divided into blank group, model group and Polygonum capitatum group. Gastritis was induced in rats by oral gavage with H. pylori ; blank group was treated with sterile Brain Heart Infusion Broth, model group and Polygonum capitatum group were first treated with indomethacin, then served to construct H. pylori infected rele- vance gastritis rats model. Blank group and model group were treated with normal saline irrigation, Po- lygonum capitatum group were treated with Polygonum capitatum irrigation for two weeks; HE staining was adopted to evaluate the Acute gastritis inflammation damage level, ELISA to test IFN-γ and IL-4 content of three groups ; real time-PCR to test relative expression level of IFN-γ mRNA and IL-4 mR- NA in mucositis. Result： After treatment, gastric inflammation in Polygonum capitatum group was im- proved obviously. The mRNA expression and the serum content of IFN-γ in Polygonum capitatum group were significantly lower than the model group, it was statistically significant （ P 〈 0.05 ）. But Polygonum capitatum had little effect on secretion IL-4 in the process of H. pylori infection. Conclusion： Polygonum capitatum could inhibit H. priori-associated gastritis probably via down-regulation of IFN-γ mRNA expression.