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目的:研究乳鹿颗粒对大鼠幽门螺杆菌(Hp)感染性胃炎的作用及可能机制。方法:用Hp菌液给大鼠灌胃制备Hp感染性胃炎模型,灌胃给药治疗结束2周后,腹主动脉取血进行血液中白介素1 beta(IL-1β)、白介素6(IL-6)、肿瘤坏死因子alpha(TNF-α)及白介素4(IL-4)、白介素10(IL-10)含量分析;取胃组织分别进行直接涂片、快速尿素酶及细菌培养实验检测细菌定植情况,光学显微镜观察胃组织病理学变化。实时定量PCR检测胃组织中巨噬细胞移动抑制因子(MIF)及对应的受体CD74基因表达,Western blot检测胃组织中MIF和核转录因子kappa B(NF-κB)p65。结果:乳鹿颗粒4.0和8.0g/kg可显著改善Hp感染性胃炎大鼠的一般状况,降低血液中促炎因子IL-1β、IL-6和TNF-α含量及胃组织中MIF、CD74和NF-κBp65的基因和蛋白表达水平,升高血液中抗炎因子IL-4、IL-10的含量,提高Hp的清除率和根除率,减轻Hp和促炎因子对胃粘膜造成损伤。结论:乳鹿颗粒对大鼠Hp感染性胃炎具有较好的保护作用,抑制MIF/CD74表达和NF-κB的核移位,进而抑制炎症因子表达可能是其作用机制之一。
Objective: To study the effect of milk deer particles on Helicobacter pylori (Hp) infectious gastritis and its possible mechanism. Methods: The model of Hp infectious gastritis was prepared by intragastric administration of Hp bacteria liquid. Two weeks after the intragastric administration, blood was collected from the abdominal aorta for determination of interleukin 1 beta (IL-1β), interleukin 6 (IL- 6, TNF-α, IL-4 and IL-10. The gastric tissues were directly smear, rapid urease and bacterial culture to detect the bacterial colonization The conditions were observed by light microscopy. Real-time quantitative PCR was used to detect the expression of macrophage migration inhibitory factor (MIF) and its receptor CD74 in gastric tissues. The expression of MIF and NF-κB p65 in gastric tissues were detected by Western blot. Results: Milk deer particles 4.0 and 8.0g / kg could significantly improve the general condition of Hp-infected gastritis rats, decrease the contents of proinflammatory cytokines IL-1β, IL-6 and TNF-α and the levels of MIF, CD74 and The gene and protein expression of NF-κBp65 increased the levels of anti-inflammatory cytokines IL-4 and IL-10 in the blood, increased the clearance rate and eradication rate of Hp, and alleviated the damage of gastric mucosa caused by Hp and proinflammatory cytokines. Conclusion: The milk deer particles have a good protective effect on Hp infectious gastritis in rats, inhibiting the expression of MIF / CD74 and NF-κB nuclear translocation, and then inhibiting the expression of inflammatory cytokines may be one of its mechanisms.