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作 者:霍黉琦[1] 李新平[1] 范开 曹志飞[1] 路冠南[1] 汪成富[1]
机构地区:[1]苏州大学生命科学学院,江苏苏州215006 [2]重庆富进生物医药有限公司,重庆400041
出 处:《中国药学杂志》2005年第22期1749-1752,共4页Chinese Pharmaceutical Journal
基 金:江苏省资源生物技术重点实验室开发基金(RBT20040504)
摘 要:目的研究重组人角质细胞生长因子(K102)在体内和体外的生物活性。方法运用3T3BALB/c细胞和大鼠CCl4肝纤维化模型对K102在体内体外的生物活性进行测定。结果体外生物活性检测:K102明显抑制成纤维细胞的生长,bFGF对K102有一定拮抗作用,且具有剂量依赖性;体内生物活性检测:治疗给药组血清ALT,AST和肝组织羟脯氨酸含量较CCl4模型组明显改善。病理组织学检查见K102大、小剂量组肝细胞脂肪变性和水样变性比较轻,汇管区纤维组织仅有轻微增生。结论K102的抗肝纤维化作用可能是通过促进肝细胞增生、合成代谢,以及抑制成纤维细胞生长、减少纤维组织增生而产生的。OBJECTIVE To study the hioaetivities of K102 in vivo and in vitro .METHODS the 3T3 BALB/c cell line and the rat model with liver fibrosis were Utilized to evaluate the bioaetivities of K102 in viro and in viro .RESULTS The proliferation of fibrohlasts was inhlhlted by K102 in vitro. A dose- dependent antagonistic effeel was found hetween K102 and hFGF. The serum levels of ALT, AST and the liver hydroxyproline level in the treated groups were lower than that in the CCl4 model group. Pathological examination showed a slight fatty degeneration and hydropie degeneration was observed in the group treated with the high dose K102, the low dose K102, and the control group. And the flbroustissue hyperplasia of the portal area in the first two groups was more slight than that in the eontrol group. CONCLUSION In viro, K102 may play an important role in anti-fihrosis by promoting the proliferation and anaholism of hepatoeytes, inhihiting the proliferation of liver fibroblasts and hyperplasia of fibroustissue.
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