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Anti-steatotic and anti-fibrotic effects of the KCa3.1 channel inhibitor, Senicapoc, in non-alcoholic liver disease 预览
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作者 Latha Paka David E Smith +10 位作者 Dawoon Jung Siobhan McCormack Ping Zhou Bin Duan Jing-Song Li Jiaqi Shi Yong-Jie Hao Kai Jiang Michael Yamin Itzhak D Goldberg Prakash Narayan 《世界胃肠病学杂志:英文版》 SCIE CAS 2017年第23期4181-4190,共10页
AIM To evaluate a calcium activated potassium channel(KCa3.1) inhibitor attenuates liver disease in models of non-alcoholic fatty liver disease(NAFLD).METHODS We have performed a series of in vitro and in vivo studies... AIM To evaluate a calcium activated potassium channel(KCa3.1) inhibitor attenuates liver disease in models of non-alcoholic fatty liver disease(NAFLD).METHODS We have performed a series of in vitro and in vivo studies using the KCa3.1 channel inhibitor, Senicapoc. Efficacy studies of Senicapoc were conducted in toxin-, thioacetamide(TAA) and high fat diet(HFD)-induced models of liver fibrosis in rats. Efficacy and pharmacodynamic effects of Senicapoc was determined through biomarkers of apoptosis, inflammation, steatosis and fibrosis. RESULTS Upregulation of KCa3.1 expression was recorded in TAA-induced and high fat diet-induced liver disease. Treatment with Senicapoc decreased palmitic aciddriven Hep G2 cell death.(P < 0.05 vs control) supporting the finding that Senicapoc reduces lipiddriven apoptosis in Hep G2 cell cultures. In animals fed a HFD for 6 wk, co-treatment with Senicapoc,(1) reduced non-alcoholic fatty liver disease(NAFLD) activity score(NAS)(0-8 scale),(2) decreased steatosis and(3) decreased hepatic lipid content(Oil Red O, P < 0.05 vs vehicle). Randomization of TAA animals and HFD fed animals to Senicapoc was associated with a decrease in liver fibrosis as evidenced by hydroxyproline and Masson’s trichrome staining(P < 0.05 vs vehicle). These results demonstrated that Senicapoc mitigates both steatosis and fibrosis in liver fibrosis models.CONCLUSION These data suggest that Senicapoc interrupts more than one node in progressive fatty liver disease by its anti-steatotic and anti-fibrotic activities, serving as a double-edged therapeutic sword. 展开更多
关键词 高胖的饮食 脂肪变性 纤维变性 KCa3.1 隧道 Senicapoc 发炎
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BRCA1在人类肿瘤细胞中的表达 预览
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作者 孟庆慧 袁仁起 +5 位作者 樊赛军 Itzhak D.Goldberg Eliot M Rosen 《实验生物学报》 CSCD 北大核心 2001年第1期 55-64,共10页
人类乳癌易感基因1(BRCA1)是乳癌,卵巢癌和前列腺癌的危险因素之一,而且表现出许多的生物功能.采用Western Blotting和半定量RT-PCR的方法,我们检测了内源性BRCA1蛋白质和mR-NA在从十一种人类肿瘤组织中建立的四十三种肿瘤细胞系的表达... 人类乳癌易感基因1(BRCA1)是乳癌,卵巢癌和前列腺癌的危险因素之一,而且表现出许多的生物功能.采用Western Blotting和半定量RT-PCR的方法,我们检测了内源性BRCA1蛋白质和mR-NA在从十一种人类肿瘤组织中建立的四十三种肿瘤细胞系的表达水平.在不同的肿瘤细胞中BR-CA1的表达水平是各不一样的.而且并没有发现BRCA1的表达和细胞的内源性p53基因状况有明显的相关性.通过采用细胞转染乳头状瘤病毒-E6致癌基因或采用畸变的p53基因(143Ala→Va1)而导致的p53基因功能失活并不对内源性BRCA1本底表达水平产生任何的影响,但两种与p53功能有关p21(-/-)和Gadd45基因剔除则轻微地增加BRCA1蛋白质的表达.因此,虽然我们目前还不清楚BRCA1在人类肿瘤细胞中不同表达的功能意义,但本文的结果为进一步研究BRCA1在不同肿瘤细胞系的生物功能提供了有价值的背景资料. 展开更多
关键词 BRCA1 P53 肿瘤细胞 基因 人类
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