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【期刊论文】IFN-a1b对肝星状细胞形态及其CTGF表达影响的研究*
汪谦, 陈伟锋, 张可飞, 黄洁夫, 徐鸿绪
中国病理生理杂志,2005,21(6):1147~1150,-0001,():
-1年11月30日
目的:通过观察IFN-alb对肝星状细胞(HSC)形态和表达CIGF的影响,探讨IFN-alb在治疗纤维化中的作用机制。方法:采用体外培养大鼠肝星状细胞,分别加入IFN-alb、TGF-β1,观察肝星状细胞的形态学及CTGF表达的改变。结果:透射电镜观察到IFN-alb作用组肝星状细胞有明显的凋亡现象发生;RT-PCR观察到正常组和1GF-β1诱导肝星状细胞表达的CTGF mRNA随IFN-alb的作用而减少。结论:IFN-alb对肝星状细胞表达CT-GF的抑制作用机制可能是通过诱导肝星状细胞凋亡和抑制TGF-β1诱导肝星状细胞表达CTGF。
肝星状细胞, 干扰素a, 结缔组织生长因子
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汪谦, 陈俊任, 梁力建, 黄洁夫
肝胆外科杂志,2004,10(5):1~4,-0001,():
-1年11月30日
目的 评价改良全肝血流阻断法在肝切除术中的安全性及应用价值。方法 回归分析近年11例常规方法不能切除的中央型肝肿瘤病例,采用全肝血流阻断法,2例同时利用静脉一静脉转流方法,1例利用体外循环静脉转流技术。结果 1例术中不能耐受全肝血流阻断术中死亡,其余10例顺利切除肿瘤,手术时间327.3±117.8min,3例术后出现右胸积液,1例心房纤颤。结论 全肝血流阻断方法对减少术中出血无优势,且术后并发症发生率高,宜仅选择性应用于肿瘤侵犯肝静脉主干、腔静脉或伴有腔静脉癌栓者。
全肝血流阻断, 肝切除术
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汪谦, Mingui Fu, Xiaojun Zhu, Qian Wang, Jifeng Zhang, Qing Song, Hui Zheng, Wataru Ogawa, Jie Du, Yuqing E. Chen
Circ Res. 2001; 89: 1058-1064.,-0001,():
-1年11月30日
Vascular diseases such as atherosclerosis are characterized by abnormal accumulation of vascular smooth muscle cells (VSMCs) within the intimal lining. The intimal VSMCs exhibit an increased expression of peroxisome proliferator-activated receptor (PPAR), and the administration of pharmacological PPAR agonists attenuates vascular lesion formation. The factors that regulate PPAR expression in the vasculature are poorly defined. Here we report that platelet-derived growth factor (PDGF) upregulates PPAR by the phosphatidylinositol 3-kinase (PI3-kinase)/Akt signaling pathway. Using Northern-blotting and Western-blotting analyses, we observed that the levels of PPAR mRNA and protein were increased by 2-to 3.5-fold in human aortic smooth muscle cells (HASMCs) treated with PDGF (20ng/mL). This was abolished by preincubation of HASMCs with a PI3-kinase inhibitor (LY294002, 50mol/L), and partially inhibited by a MEK1 inhibitor (U0126, 10mol/L), but not affected by a p38 kinase inhibitor (SB202190, 10mol/L). In addition, overexpression of the dominant-negative p85 subunit of PI3-kinase or Akt proteins blocked the PDGF-induced PPAR expression. Taken together, our results suggest that PDGF induces PPAR expression in VSMCs by a PI3-kinase/Akt signaling pathway. The characterization of factors and signaling pathways that modulate PPAR expression in VSMCs may have important implications for understanding the pathogenesis of vascular diseases.
platelet-derived growth factor, peroxisome proliferator-activated receptor, phosphatidylinositol 3-kinase, signaling pathway, vascular smooth muscle cells
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