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作 者:李德旭[1] 周晟[2] 王新保 李大鹏 邓小荣 杨镇[1] 裘法祖[1]
机构地区:[1]华中科技大学同济医学院附属同济医院普外科,武汉430030 [2]华中科技大学同济医学院附属同济医院病理科,武汉430030
出 处:《华中科技大学学报(医学版)》2002年第1期47-49,共3页Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
基 金:国家自然科学基金资助项目 (No.39470 6 85 )
摘 要:对 34例门脉高压患者的肝内外血管与 30例对照组织行 HE染色观察形态学变化 ;行蛋白激酶 Cα (PKCα)免疫组化染色并行定量分析。结果发现门脉高压患者肝外血管呈门脉高压性血管病变 ,肝内有微循环障碍。正常肝内外血管 PKCα免疫组化染色呈阴性或弱阳性 ,门脉高压患者的肝脏和脾动静脉呈强阳性 ,定量分析二者差异有显著性 (P<0 .0 1)。提示 :PKCα过度表达可能是门脉高压肝内外血管结构改变的重要原因 ,并可能改变其血管舒缩活性物质的合成及敏感性。The expression of PKCα in spleen artery and vein and intrahepatic vessels of 34 patients with portal hypertension was detected by using immunochemistry staining. Morphological changes was observed in the samples from spleen artery and vein and intrahepatic vessels of 34 patients with portal hypertension and 30 controls following HE staining. The results showed that PKCα was not detectable in normal vessels and was highly expressed in spleen artery and vein and intrahepatic vessels of patients with portal hypertension with the difference being statistically significant (P<0.01). The expression of PKCα in spleen artery and vein and intrahepatic vessels of patients with portal hypertension was increased and could enhance the proliferation of SMC. PKC signal transduction might be engaged in the formation of portal hypertension by regulating the proliferation of vein SMC, vascular remodeling and vascular tension, and PKCα might play a very important role in the portal hypertension.
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