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梗阻性黄疸鼠肝脏血红素氧化酶-1及一氧化碳含量的研究
引用本文:丁佑铭,程邦昌,戴峰,谭海燕. 梗阻性黄疸鼠肝脏血红素氧化酶-1及一氧化碳含量的研究[J]. 中华实验外科杂志, 2003, 20(12): 1081-1082
作者姓名:丁佑铭  程邦昌  戴峰  谭海燕
作者单位:1. 430060,武汉大学人民医院普外科
2. 湖北省老河口市人民医院外科
基金项目:湖北省教育厅重点科研基金资助项目(2003X121)
摘    要:目的 探讨梗阻性黄疸时肝脏血红素氧化酶-1(HO-1)及血浆中一氧化碳(CO)含量的变化。方法 48只 Wistar 大鼠随机分为 4组:假手术对照组(CG)、梗阻性黄疸 7 d组(7 d)、梗阻性黄疸 14 d组(14 d)和梗阻性黄疸 21 d组(21 d),采用免疫组织化学法对肝细胞中 HO-1表达进行分析,应用双波长分光光度计法测定大鼠肝静脉、门静脉及下腔静脉血浆中CO含量。结果 梗阻性黄疸时 HO-1不仅在 Kupffer细胞中表达,而且在肝实质细胞中呈弥漫性表达上调,14 d组和 21 d组肝实质细胞中HO-1表达均较7 d组增加(P<0.01)。梗阻性黄疸各组肝静脉血浆中CO含量较CG组增高(P<0.05,P<0.01);14 d组门静脉血浆中CO含量升高明显,与CG组比较差异有显著性(P<0.05);梗阻性黄疸各组肝静脉血浆中 CO含量与同时间组门静脉血浆中 CO含量相比均显著升高(P<0.01)。梗阻性黄疸各时间组肝静脉CO含量的增高与肝实质细胞中HO-1表达的变化呈显著正相关(P<0.01)。结论 梗阻性黄疸时肝细胞HO-1表达上调致CO产生增多,从而有助于增加肝血流量并减少肝脏功能损害。

关 键 词:梗阻性黄疸 肝脏 血红素氧化酶-1 一氧化碳 大鼠 免疫组织化学
修稿时间:2003-02-25

Altered expression of hene oxygenase-1 in the livers and blood carbon monoxide level of rats with obstructive jaundice
DING You-ming,CHENG Bang-chang,DAI Feng,et al.. Altered expression of hene oxygenase-1 in the livers and blood carbon monoxide level of rats with obstructive jaundice[J]. Chinese Journal of Experimental Surgery, 2003, 20(12): 1081-1082
Authors:DING You-ming  CHENG Bang-chang  DAI Feng  et al.
Affiliation:DING You-ming,CHENG Bang-chang,DAI Feng,et al. Department of General Surgery,Renmin Hospital of Wuhan University,Wuhan 430060,China
Abstract:Objective To investigate the effect of altered hepatic heme oxygenase--1 (HO--1) ex-pression and blood carbon monoxide (CO) level on hepatic function in obstructive jaundice. MethodsForty-eight Wister rats were divided randomly into control group (CG), bile duct ligation 7--day group(7 d), bile duct ligation 14--day group (14 d) and bile duct ligation 21--day group (21 d). Immunohisto-chemistry and double--wavelength spectrophotometer were employed to detect the expression of HO-1 pro-tein in hepatocytes and the blood CO levels in the hepatic vein, the portal vein and the inferior vena cava.Results HO-1 was expressed only in kupffer cells of the liver in CG group. But the rats with jaundice,HO-1 was expressed in kupffer cells as well as parenchymal liver cells, and the HO-1 expression levels ofthe parenchymal liver cells in 14 d group and 21 d group were increased more significantly than that in 7d group (P < 0. 05, P < 0. 01). There was a significant increase of the CO level of hepatic vein in the ratswith jaundice in contrast to CG group (P < 0. 05, P < 0. 01). As compared with CG group, the CO levelof portal vein in 14 d group was significantly increased (P < 0. 05). The CO level of hepatic vein washigher than that of portal vein after ligating common bile duct (P < 0. 01). There was a significant posi-tive correlation between the CO levels of hepatic vein and altered HO--1 expression of parenchymal livercells in jaundiced rats (P < 0. 01). Conclusion Up--regulation of HO-1 expression of parenchymal livercells in obstructive jaundice and following high levels of hepatic CO could increase hepatic blood flow, thusleading to the alleviation of hepatic dysfunction in obstructive jaundice.
Keywords:Jaundice  Heme oxygenase-1  Carbon monoxide
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