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机构地区:[1]郑州大学医药科学研究院,河南郑州450052 [2]河南中医学院,河南郑州450008
出 处:《中成药》2009年第7期1000-1003,共4页Chinese Traditional Patent Medicine
基 金:河南省属院所预研专项基金资助课题(082103810403)
摘 要:目的:观察姜黄素(Curcumin)在四氯化碳(CCl4)诱导大鼠肝纤维化中,对肝组织核因子-κB(NF-κB)激活与过氧化物酶体增殖物激活受体-γ(PPAR-γ)表达的影响。方法:60只雄性清洁级SD大鼠随机分为正常对照组、模型组、阳性药物水飞蓟组、姜黄素低、中、高剂量组,采用皮下注射40%CCI4复制模型,自8周开始水飞蓟组大鼠给予50 mg/kg,姜黄素治疗组大鼠分别给予的剂量为100、200、400 mg/kg,灌胃6周。HE染色观察观察肝组织在光镜下的病理改变并进行肝纤维化分级;免疫组织化学测定NF-κB的表达变化;RT-PCR检测PPAR-γmRNA表达。结果:姜黄素治疗组大鼠肝脏的炎症反应和纤维化的病理改变较模型组显著减轻(P<0.01)。姜黄素治疗组大鼠肝脏NF-κB活性与模型组相比明显降低,差异显著(P<0.05),模型组PPAR-γmRNA表达较正常组及姜黄素用药组显著减弱(P<0.05)。结论:姜黄素可明显的抗CCl4诱导的大鼠肝纤维化效应,其抗肝纤维化的机制与PPAR-γ配体激活PPAR-γ的表达的同时,抑制NF-κB的活性有关。AIM : To investigate the effect of curcumin on the binding activity of hepatic nuclear factor-kappa B (NF-KB) and the expression of peroxisome proliferator-activated receptor-γ(PPAR-γ) in rats with liver fibrosis induced by carbon tetrachoride. METHODS: A total of 60 clean male rats were randomly and averagely divided into group A, B, C, D, E and F. The rats in group A served as normal controls, while those in other five groups were injected subcutaneously 40% CCI4 for seven weeks to induce the model of liver fibrosis. After seven weeks, the rats in group C, D, E, F were intragastrically administered with 50 mg/kg silibinin, 100 mg/kg cur, 200 mg/kg cur, 400 mg/kg cur once per day for six weeks, respectively. HE staining was used to observe the pathological changes of liver tissues under light microscope, and immunohistochemistry and reverse transcriptase polymerase chain reaction (RT-PCR) were performed to detect the activity of NF-kB, PPAR-γ and mRNA expression of PPAR-γ. RESULTS:The inflammatory and fibrotic degrees were obviously alleviated in group C, D, and E compared with group B. The expression of NF-kB p65 was significantly decreased in liver tissue in group C, D and E, compared with model control group B ( P 〈 0.05 ). The expression of PPAR-γ mRNA was significantly enhanced, as compared with model control group B(P 〈 0.05 ). CONCLUSION: NF-KB and PPAR-γ may be involved in the pathogenesis of liver fibrosis induced by carbon tetrachoride. Curcumin, a ligand of PPAR-γ, is obviously effective in the treatment of this disease by up-regulating PPAR-γ expression and reducing NF-kB activity.
关 键 词:姜黄素 肝纤维化 核因子-ΚB 过氧化物酶体增殖物激活受体Γ
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