出 处:《中医药导报》2021年第11期25-29,共5页Guiding Journal of Traditional Chinese Medicine and Pharmacy
基 金:河北省医学科学研究计划(20201528)。
摘 要:目的:探讨蒲公英甾醇对Hp相关性胃炎脾胃湿热证(HAG)小鼠改善和炎症抑制作用及机制。方法:80只C57BL/6小鼠随机分为正常组17只和造模组63只,正常组小鼠给予正常饮食+常规环境+同步饲养,造模组小鼠给予肥甘饮食+湿热环境+Hp菌液,制备HAG小鼠模型。将48只造模成功的小鼠随机分为模型组、蒲公英甾醇组、iE-DAP组和蒲公英甾醇+iE-DAP组,每组12只。蒲公英甾醇组小鼠灌胃蒲公英甾醇,5mg/kg,1次/d,连续灌胃4周;iE-DAP组小鼠腹腔注射iE-DAP,100μg/只,1次/周,连续注射4周;蒲公英甾醇+iE-DAP组小鼠灌胃蒲公英甾醇,5 mg/kg,1次/d,腹腔注射iE-DAP,100μg/只,1次/周,连续给药4周。实验过程中观察小鼠一般情况;ELISA检测小鼠血清干扰素诱导蛋白10(IP-10)和干扰素β(IFN-β)水平;快速尿素酶实验检测Hp定植;HE染色镜检小鼠胃黏膜组织病理学变化;qRT-PCR检测小鼠胃组织中核苷酸结合寡聚化结构域1(NOD1)mRNA和受体相互作用蛋白2(RIP2)mRNA表达水平;Western blotting检测小鼠胃黏膜组织p65、p-p65蛋白表达水平。结果:正常组小鼠胃黏膜组织结构完整、排列整齐、无炎症细胞浸润及充血肿胀;模型组小鼠出现脾胃湿热证症状,胃黏膜充血肿胀、结构破坏、排列无序、固有层有炎症细胞浸润;蒲公英甾醇组小鼠症状较模型组好转,胃黏膜病理损伤减轻;iE-DAP组小鼠脾胃湿热症状、胃黏膜组织病理损伤较模型组加重,蒲公英甾醇+iE-DAP组小鼠组脾胃湿热症状、胃黏膜组织病理损伤明显减轻。与模型组比较,蒲公英甾醇组小鼠血清IP-10和IFN-β水平,NOD1 mRNA和RIP2 mRNA相对表达量,以及p-p65蛋白表达降低,且HP定植减少(P<0.05),iE-DAP组小鼠血清IP-10和IFN-β水平,NOD1 mRNA和RIP2 mRNA相对表达量,以及p-p65蛋白表达升高,且Hp定植增加(P<0.05);与蒲公英甾醇组比较,蒲公英甾醇+iE-DAP组小鼠血清IP-10和IFN-β水平,NOD1 mRNA和RIP2 mRNA相对表达量,以及pObjective: To investigate the effect and mechanism of taraxasterol on the improvement and inflammation inhibition of Hp-associated gastritis(HAG) mice with spleen stomach damp heat syndrome. Methods:80 C57 BL/6 mice were randomly divided into normal group, and model group, with 17 in normal group and 63 in model group. The mice in the normal group were given normal diet + conventional environment + synchronous feeding, and the mice in the model group were given fat and sweet diet + hot and humid environment + Hp bacterial solution to prepare the HAG mice model. After successful modeling, 48 successful mice were randomly divided into taraxasterol group, iE-DAP group, taraxasterol + iE-DAP group, with 12 mice in each group. Taraxasterol group was gavaged 5 mg/kg taraxasterol once a day for 4 weeks. iE-DAP group was intraperitoneally injected with iE-DAP 100 μg/mice, once a week, for consecutive 4 weeks;taraxasterol + iE-DAP group was gavaged 5 mg/kg taraxasterol once a day, and iE-DAP was intraperitoneally injected 100 μg/mice once a week for 4 weeks. The general condition of mice was observed during the experiment. Serum levels of interferon-induced protein 10(IP-10) and interferon β(IFN-β) were determined by ELISA. HP colonization was detected by rapid urease assay. The histopathological changes of gastric mucosa were examined by HE staining. The relative mRNA expression levels of nucleotide binding oligomerization domain 1(NOD1) and receptor-interacting protein 2(RIP2)in mice stomach tissues were detected by qPCR. The protein expression levels of p65 and p-p65 in gastric mucosa of mice were detected by Western blotting. Results: The structure of gastric mucosa in normal group was intact and orderly, and there was no inflammatory cell infiltration, congestion and swelling. Model group showed symptoms of dampness-heat syndrome of spleen and stomach, congestion and swelling of gastric mucosa, structural destruction, disordered arrangement, and infiltration of inflammatory cells in lamina propria. The symptoms o
关 键 词:HP相关性胃炎 脾胃湿热证 蒲公英甾醇 核苷酸结合寡聚化结构域1/核因子κB通路 小鼠
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