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作 者:姜惠芳[1] 余学清[1] 姜宗培[1] 李晓艳[1] 陈伟英[1]
机构地区:[1]中山大学附属第一医院肾内科//教育部重点实验室,广东广州510080
出 处:《中山大学学报(医学科学版)》2005年第3期264-267,共4页Journal of Sun Yat-Sen University:Medical Sciences
摘 要:【目的】探讨己酮可可碱对转化生长因子鄄β1诱导的大鼠腹膜间皮细胞胶原ⅠmRNA表达及细胞外信号调节激酶活性的影响。【方法】用逆转录鄄聚合酶链反应检测腹膜间皮细胞胶原ⅠmRNA表达,用Westernblot检测磷酸化细胞外信号调节激酶。【结果】①0.3mg/mL己酮可可碱与对照组相比,可下调胶原ⅠmRNA表达32%(P<0.01),其抑制作用呈时间依赖性关系,作用16h抑制作用达高峰(0.790vs0.426,P<0.001)。②TGF鄄β1可诱导腹膜间皮细胞胶原ⅠmRNA表达上调(132.00vs592.00,P<0.001),以及磷酸化细胞外信号调节激酶表达增加(201.67vs682.00,P<0.001)。③己酮可可碱可抑制TGF鄄β1诱导的腹膜间皮细胞胶原ⅠmRNA表达上调(0.945vs0.594,P<0.01),并可逆转TGF鄄β1诱导的磷酸化细胞外信号调节激酶表达增加(682.00vs426.00,P<0.001),其抑制作用呈剂量依赖关系。【结论】己酮可可碱可下调腹膜间皮细胞胶原ⅠmRNA的基础表达及TGF鄄β1诱导的过度表达,同时可逆转TGF鄄β1诱导的腹膜间皮细胞细胞外信号调节激酶活性增加。Objective]To investigate the effect of pentoxifylline (PTX) on type Ⅰcollagen mRNA expression and extracellular signal-regulated kinase (ERK) activation induced by transforming growth factor-beta1 (TGF-β1) in rat peritoneal mesothelial cells. [Methods]The expression of type Ⅰ collagen mRNA was measured with RT-PCR. Phosphorylated ERK was detected by Western blotting. [Result] (1) 0.3 mg/mL PTX inhibited the typeⅠ collagen mRNA by 32% (P< 0.01) in time-dependent manner. The peak of inhibition was at 16 hr (0.790 vs 0.426, P<0.001). (2) TGF-β1 increased the expression of typeⅠ collagen mRNA (132.00 vs 592.00, P< 0.001) and the phosphorylated ERK expression (201.67 vs 682.00, P< 0.001) in the rat peritoneal mesothelial cells. (3) PTX inhibited the overexpression of the typeⅠ collagen mRNA induced by TGF-β1 in the peritoneal mesothelial cells (0.945 vs 0.594, P< 0.01) and also reversed the increase of phosphorylated ERK expression (682.00 vs 426.00, P<0.001) in dose-dependent manner. [Conclusion] PTX could down regulate the basic expression and overexpression of typeⅠ collagen mRNA induced by TGF-β1 and reverse the increase of phosphorylated ERK induced by TGF-β1 in the rat peritoneal mesothelial cells. So PTX may prevent or treat peritoneal fibrosis in CAPD patients.
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