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目的评估重组人乳铁蛋白(rhLF)对幽门螺杆菌(H.pylori)的抑菌作用及其对细胞毒素相关蛋白A(CagA)、尿素酶(Ure)和胃黏膜白细胞介素8(IL-8)的影响。方法测定最低抑菌浓度(MIC)和不同药物浓度对H.pylori增殖的影响。通过实时定量PCT和Western blot检测rhLF对H.pylori CagA和Ure的mRNA和蛋白表达的影响。动物实验,144只BABL/c小鼠,分为4组,标准三联+rhLF组(A组)、rhLF组(B组)、标准三联组(C组)、生理盐水组(D组),组织病理学苏木素-伊红(HE)染色观察不同分组间胃黏膜炎性反应,ELISA法检测各组胃组织IL-8水平。结果 MIC为0.5mg/mL,且rhLF抑制细菌生长增殖呈现浓度依赖性过程。rhLF能降低H.pylori主要毒力因子CagA、Ure mRNA和蛋白的表达。A组胃黏膜组织炎症积分和匀浆液IL-8水平与B、C、D组比较,差异均有统计学意义(P<0.05)。结论 rhLF抑制H.pylori生长及增殖,并不同程度抑制H.pylori主要毒力因子CagA、Ure mRNA及蛋白的表达,削弱该菌的致病性,同时降低小鼠胃黏膜IL-8水平,减轻H.pylori相关性胃黏膜炎性反应。
Objective To evaluate the bacteriostasis of recombinant human lactoferrin (rhLF) against H.pylori and its effects on the cytotoxicity of CagA, Ure and interleukin-8 (IL- 8) the impact. Methods The effect of MIC and different drug concentrations on the proliferation of H.pylori were determined. The effect of rhLF on mRNA and protein expression of CagA and Ure of H.pylori was detected by real-time quantitative PCR and Western blot. Animal experiments, 144 BABL / c mice were divided into 4 groups: standard triple + rhLF group (group A), rhLF group (group B), standard triple group (group C), saline group (group D) Pathology The hematoxylin-eosin (HE) staining was used to observe the gastric mucosal inflammatory response in different groups. The levels of IL-8 in gastric tissues were detected by ELISA. Results MIC was 0.5 mg / mL, and rhLF inhibited bacterial growth and proliferation in a concentration-dependent manner. rhLF can reduce the expression of CagA, Ure mRNA and protein, the main virulence factors of H.pylori. Gastric mucosal inflammation score and homogenate IL-8 level in group A were significantly different from those in groups B, C and D (P <0.05). Conclusions rhLF can inhibit the growth and proliferation of H.pylori and inhibit the expression of CagA and Ure mRNA and protein of H. pylori, which are the major virulence factors of H.pylori to a certain extent, impair the pathogenicity of the bacteria and reduce the level of IL-8 in gastric mucosa H.pylori-related gastric mucosal inflammatory response.