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目的:观察蒿芩清胆汤对幽门螺杆菌感染小鼠胃黏膜核转录因子κB p65(NF-κBp6)、白细胞介素-8(IL-8)、诱导型一氧化氮合酶(iNOS)表达的影响,探讨其治疗幽门螺杆菌相关性胃炎(HAG)的作用机制。方法:按照性别、体重随机抽取10只小鼠作为空白对照组,其余60只小鼠采用幽门螺杆菌(Hp)标准菌株(SS1)布氏肉汤液灌胃造模,建立Hp感染小鼠模型。造模成功后,将其随机分为6组,每组10只,分别为丽珠胃三联组、三九胃泰组、模型组、蒿芩清胆汤高、中、低剂量组,每组小鼠灌服相应药液,空白组、模型组小鼠灌服等量生理盐水,每天1次。2周后处死动物,观察各组小鼠胃黏膜病理改变,采用免疫组化法检测其胃黏膜NF-κBp6、IL-8、iNOS表达情况。结果:与模型组比较,蒿芩清胆汤能显著降低小鼠胃黏膜炎症面积,降低胃黏膜NF-κBp6、IL-8、iNOS表达,差异具有统计学意义(P<0.05)。结论:蒿芩清胆汤能减轻Hp感染小鼠胃黏膜炎症,其作用机制可能与抑制NF-κBp6炎症通路激活,下调IL-8、iNOS过度表达有关。
Objective: To observe the expression of NF-κB p65, IL-8 and inducible nitric oxide synthase (iNOS) in gastric mucosa of Helicobacter pylori-infected mice with Haoqin Qing Dan Decoction To explore its mechanism of action in the treatment of Helicobacter pylori-associated gastritis (HAG). Methods: Ten mice were randomly selected as the control group according to their sex and weight. The remaining 60 mice were intragastrically administered with the Buchner Broth of the standard strain (SS1) of Helicobacter pylori (Hp) to establish a mouse model of Hp infection . After the success of modeling, they were randomly divided into 6 groups of 10, respectively, Livzon stomach Sanlian group, Sanjiuweitai group, model group, Haoqin Qing Dan Tang high, medium and low dose groups, each group Mice fed the corresponding liquid medicine, the blank group, the model group mice were fed the same amount of saline, 1 times a day. After 2 weeks, the animals were sacrificed and the pathological changes of gastric mucosa in each group were observed. The expressions of NF-κBp6, IL-8 and iNOS in gastric mucosa were detected by immunohistochemistry. Results: Compared with the model group, Haoqin Qingdan Decoction could significantly reduce the area of gastric mucosal inflammation and reduce the expression of NF-κBp6, IL-8 and iNOS in gastric mucosa. The difference was statistically significant (P <0.05). CONCLUSION: Haoqin Qingdan Decoction can relieve gastric mucosal inflammation in Hp-infected mice, and its mechanism may be related to the inhibition of the activation of NF-κBp6 pathway and the down-regulation of IL-8 and iNOS overexpression.