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

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。

Altered expression of hene oxygenase-1 in the livers and blood carbon monoxide level of rats with obstructive jaundice

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. Methods Forty-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 of the parenchymal liver cells in 14 d group and 21 d group were increased more significantly than that in 7 d group (P < 0. 05, P < 0. 01). There was a significant increase of the CO level of hepatic vein in the rats with jaundice in contrast to CG group (P < 0. 05, P < 0. 01). As compared with CG group, the CO level of portal vein in 14 d group was significantly increased (P < 0. 05). The CO level of hepatic vein was higher 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 liver cells in jaundiced rats (P < 0. 01). Conclusion Up--regulation of HO-1 expression of parenchymal liver cells in obstructive jaundice and following high levels of hepatic CO could increase hepatic blood flow, thus leading to the alleviation of hepatic dysfunction in obstructive jaundice.