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肝纤维化大鼠血小板衍生生长因子受体β亚单位的表达及其与细胞外基质成分的相关性
引用本文:陆翠华,陈岳祥,张忠兵,谢渭芬,黄介飞,倪润洲,郭亚军,卫立辛,金由辛.肝纤维化大鼠血小板衍生生长因子受体β亚单位的表达及其与细胞外基质成分的相关性[J].中华肝脏病杂志,2004,12(11):663-665.
作者姓名:陆翠华  陈岳祥  张忠兵  谢渭芬  黄介飞  倪润洲  郭亚军  卫立辛  金由辛
作者单位:1. 226001,江苏南通医学院附属医院消化科
2. 上海第二军医大学长征医院消化科
3. 上海第二军医大学国际合作肿瘤研究所
4. 中国科学院上海生物化学研究所
基金项目:国家自然科学基金(39870303)
摘    要:目的 研究血小板衍生生长因子(PDGF)受体β亚单位在肝纤维化组织中的动态表达及其与细胞外基质成分的相关性。 方法 将动物分为正常对照组和模型组,用C Cl4复制肝纤维化模型,用免疫组化方法动态检测PDGF受体β亚单位、α~平滑肌抗体(α-SMA)、Ⅰ、Ⅲ型胶原在肝纤维化组织中的表达,将免疫组化结果行图像扫描半定量后进行统计学分析并计算其相关性。 结果 随着肝纤维化程度的加重,PDGF受体β亚单位、α—SMA表达逐渐增加,Ⅰ、Ⅲ型胶原的表达也逐步增加。在2周时PDGF受体β亚单位与Ⅰ、Ⅲ型胶原的相关性不明显,但与α-SMA呈显著相关,其相关系数为0.6 2(P<0.05);在4周时其与Ⅰ、Ⅲ型胶原和α—SMA的相关系数分别为0.74、0.60和0.69(P<0.05);在6周时其与Ⅰ、Ⅲ型胶原和α-SMA的相关系数分别为0.83、0.67和0.81(P<0.05)。 结论 PDGF受体β亚单位在肝纤维化的发生发展中起重要作用,抑制PDGF受体β亚单位的表达可望能减少细胞外基质的合成。

关 键 词:肝纤维化  大鼠  血小板衍生生长因子  受体β亚单位  基因表达  细胞外基质
修稿时间:2003年11月24

The expression of platelet-derived growth factor (PDGF) receptor- β and its correlation with extracellular matrix in hepatic tissue in hepatic fibrosis rats
CHEN Yue-xiang,ZHANG Zhong-bing,XIE Wei-fen,HUANG Jie-fei,NI Run-zhou,GUO Ya-jun,WEI Li-xin,JIN You-xin. '.The expression of platelet-derived growth factor (PDGF) receptor- β and its correlation with extracellular matrix in hepatic tissue in hepatic fibrosis rats[J].Chinese Journal of Hepatology,2004,12(11):663-665.
Authors:CHEN Yue-xiang  ZHANG Zhong-bing  XIE Wei-fen  HUANG Jie-fei  NI Run-zhou  GUO Ya-jun  WEI Li-xin  JIN You-xin '
Institution:Department of Gastroenterology, Affiliated Hospital of Nantong Medical University, Jiangsu Province, Nantong 226001, China.
Abstract:OBJECTIVE: To investigate the expression of PDGF receptor-beta and its correlation with extracellular matrix in hepatic tissue during hepatic fibrosis. METHODS: The model of hepatic fibrosis in rats was induced by carbon tetrachloride. PDGF receptor-beta subunit, collagen I, collagen III and a-SMA in hepatic tissues of these rats were examined using immunohistochemistry. The correlation between PDGF receptor-beta subunit and collagen I, III was analyzed using SAS software after the results of immunohistochemistry were semi-quantified. RESULTS: PDGF receptor-beta subunit and a-SMA were not detected in normal controls. Collagen I and III were distributed in the portal tracts and beneath the endothelia of the central veins and of the Disse spaces. Two weeks after CCl4 injection, the PDGF receptor-beta and a-SMA were detected, and the expression of collagen I and III increased. At the end of 4 and 6 weeks, the above four proteins were further increased. Two weeks after CCl4 injection, PDGF receptor-beta had no apparent correlation with collagen I and III. However, PDGF receptor-beta had a significant correlation with collagen I and III 2 weeks later, and the correlation coefficient was 0.74 and 0.60 respectively at 4 weeks, and 0.83 and 0.67 respectively at 6 weeks. PDGF receptor-beta had a significant correlation with a-SMA during the whole process of hepatic fibrosis and the correlation coefficient was 0.62, 0.69 and 0.81, respectively at the time of 2, 4 and 6 weeks after CCl4 injection. CONCLUSION: The PDGF receptor-beta was overexpressed during the process of hepatic fibrosis development, and it significantly correlated with collagen I and collagen III.
Keywords:Hepatic fibrosis  Platelet-derived growth factor  Hepatic stellate cell
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