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作 者:李俊峰[1] 舒建昌[2] 杨钦河 马民 张玉佩 颜显欣
机构地区:[1]暨南大学附属第一医院消化科,广东广州510630 [2]暨南大学附属第四医院消化科,广东广州510175 [3]暨南大学中医学院,广东广州510632
出 处:《中国病理生理杂志》2017年第12期2259-2263,共5页Chinese Journal of Pathophysiology
基 金:广东省中医药局资助项目(No.20141069)
摘 要:目的:观察大叶茜草素(mollugin)对大鼠肝星状细胞系CFSC-2G活化和胶原合成的影响并探讨其分子机制。方法:小剂量(10μmol/L)过氧化氢(H_2O_2)诱导CFSC-2G细胞30 min后,再加入不同浓度(0、20、40、60和120μmol/L)的mollugin处理。MTT法检测细胞活力,real-time PCR和Western blot法分别检测核因子E2相关因子2(Nrf2)、血红素加氧酶-1(HO-1)、核因子κB(NF-κB)p65、Bcl-2、Bcl-x L、Bax以及肝星状细胞活化标志物α-平滑肌肌动蛋白和Ⅰ型胶原蛋白的mRNA和蛋白表达,并用Western blot法检测p38丝裂原活化蛋白激酶(p38MAPK)的磷酸化水平。结果:低剂量H_2O_2可以诱导CFSC-2G细胞活化,mollugin明显促进p38 MAPK磷酸化,上调Nrf2和HO-1的mRNA和蛋白表达,下调NF-κB p65、Bcl-2和Bcl-x L的mRNA和蛋白表达,抑制H_2O_2诱导活化的CFSC-2G细胞活力和胶原合成(P<0.05)。结论:Mollugin可能通过上调Nrf2和HO-1并下调NF-κB p65和Bcl-2表达,抑制CFSC-2G细胞活化和胶原合成。AIM: To investigate the effects of mollugin on the viability and collagen synthesis of rat hepatic stellate cell line CFSC-2G. METHODS: The activation of CFSC-2G cells was induced with low concentration (10 (jimol/L) of hydrogen peroxide ( H2 02) for 30 min in the experiment. The viability of the CFSC-2G cells after exposed to mollu-gin at different concentrations (0, 20, 40, 60 and 120 jjimol/L) was detected by MTT assay. The mRNA and protein ex-pression levels of nuclear factor E2-related factor 2 ( Nrf2) , heme oxygenase-1 ( HO-1) , nuclear factor-KB (NF-kB) p65 ,Bel-2, Bcl-xL, Bax, and hepatic stellate cell activation markers a-smooth muscle actin (a-SMA) and collagen type I ( Col I ) were detected by real-time PCR and Western blot. The phosphorylation level of p38 mitogen-activated protein kinase (p38 MAPK) was determined by Western blot. RESULTS : Mollugin significantly inhibited the viability and collagen syn-thesis of activated CSFC-2G cells induced by H202. The expression of Nrf2, HO-1 and Bax at mRNA and protein levels, and the phosphorylation level of p38 MAPK were promoted, while the levels of NF-kB p65, Bel-2, Bcl-xL, a-SMA and Col I were inhibited by mollugin ( P 〈 0. 05 ) . CONCLUSION : Mollugin may inhibit H2 0 2 -induced viability and collagen synthesis of the CSFC-2G cells by activating Nrf2 and HO-1 , and blocking the NF-kB p65 and Bcl-2 expression.
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