| 引用本文: | 张波,谈仁秀,黄芝月,李静,王建玲,张蓓蓓,宋文婷.MMI-0100对DDC诱导的胆汁淤积性肝损伤的治疗作用研究[J].中国现代应用药学,2022,39(13):1692-1697. |
| ZHANG Bo,TAN Renxiu,HUANG Zhiyue,LI Jing,WANG Jianling,ZHANG Beibei,SONG Wenting.Study on Therapeutic Effect of MMI-0100 Against DDC-induced Cholestatic Liver Injury[J].Chin J Mod Appl Pharm(中国现代应用药学),2022,39(13):1692-1697. |
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| MMI-0100对DDC诱导的胆汁淤积性肝损伤的治疗作用研究 |
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张波1, 谈仁秀1, 黄芝月1, 李静1, 王建玲1, 张蓓蓓1, 宋文婷2
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1.徐州医科大学, 病原生物学与免疫学教研室, 江苏省免疫与代谢重点实验室, 徐州市感染与免疫重点实验室, 江苏 徐州 221004;2.徐州医科大学, 口腔医学院, 江苏 徐州 221004
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| 摘要: |
| 目的 探讨MMI-0100对3，5-二乙氧基羰基-1，4-二氢-2，4，6-三甲基吡啶（DDC）诱导的小鼠胆汁淤积性肝损伤的治疗作用。方法 15只Balb/c小鼠随机分为对照组、模型组（DDC），治疗组（DDC+MMI-0100），每组5只。对照组小鼠给予正常饮食2 周，其余2组小鼠给予0.1% DDC饮食喂养1周后，再给予正常饮食1周，同时治疗组小鼠在DDC饲养1周后，每天经腹腔注射MMI-0100进行治疗，注射量剂量为500 μg·kg-1，连续注射1 周；对照组和模型组小鼠给予等量无菌生理盐水。观察并记录各组小鼠肝脏大体情况，HE和Masson染色观察肝脏的病理改变，免疫组化检测胆管增生指标CK19和Ki67，实时定量PCR检测肝脏纤维化相关基因α-SMA的表达。结果 与模型组相比，治疗组小鼠肝脏纤维化病变减轻（P<0.01），炎症细胞浸润减少（P<0.01），肝脏组织Knodell Score评分降低（P<0.01），同时胆管增生相关指标CK19和Ki67表达降低（P<0.05），肝脏α-SMA的mRNA表达水平降低（P<0.01）。结论 MMI-0100对DDC诱导的小鼠原发性硬化性胆管炎有良好的治疗作用。 |
| 关键词: MMI-0100 胆汁淤积 治疗作用 |
| DOI：10.13748/j.cnki.issn1007-7693.2022.13.005 |
| 分类号:R965.2 |
| 基金项目:江苏省自然科学基金项目（BK20201011）；江苏省高校自然科学研究项目（20KJB310011）；江苏省博士后基金项目（RC7062005）；江苏省研究生创新计划（KYCX20-2468） |
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| Study on Therapeutic Effect of MMI-0100 Against DDC-induced Cholestatic Liver Injury |
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ZHANG Bo1, TAN Renxiu1, HUANG Zhiyue1, LI Jing1, WANG Jianling1, ZHANG Beibei1, SONG Wenting2
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1.Xuzhou Medical University, Department of Pathogenic Biology and Immunology, Jiangsu Key Laboratory of Immunity and Metabolism, Xuzhou Key Laboratory of Infection and Immunity, Xuzhou 221004, China;2.Xuzhou Medical University, School of Stomatology, Xuzhou 221004, China
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| Abstract: |
| OBJECTIVE To explore the therapeutic effect of MMI-0100 on 3,5-diethoxycarboxyl-1,4-dihydro-2,4, 6-trimethylpyridine(DDC)-induced cholestatic liver injury in mice. METHODS Fifteen Balb/c mice were randomly divided into control group, model group(DDC) and treatment group(DDC+MMI-0100). There were 5 mice in each group. Mice in control group were fed with normal diet for 2 weeks, and mice in other two groups were fed with 0.1% DDC diet for 1 week and then given normal diet for another one week. After DDC diet for 1 week, mice in treatment group were intraperitoneally injected with 500 μg·kg-1 of MMI-0100 every day for 1 week. Mice in control group and model group were given the same amount of sterile normal saline. The general conditions of liver of mice in each group were observed and recorded. The pathological changes of liver were observed by HE and Masson staining. Markers of biliary duct hyperplasia CK19 and Ki67 were detected by immunohistochemistry. The expression of α-SMA gene which related to liver fibrosis was detected by real-time quantitative PCR. RESULTS Compared with model group, liver fibrosis, inflammatory cell infiltration and the Knodell Score of mice all reduced significantly in the treatment group(P<0.01). In addition, the bile duct hyperplasia associated markers CK19 and Ki67 also decreased in the treatment group(P<0.05), and the mRNA expression level of α-SMA in liver was decreased(P<0.01). CONCLUSION MMI-0100 has a good therapeutic effect on DDC-induced mouse primary sclerosing cholangitis. |
| Key words: MMI-0100 cholestasis therapeutic effect |
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