熊脱氧胆酸促进肝脏部分切除后肝细胞再生

目的 探讨熊脱氧胆酸（ｕｒｓｏｄｅｏｘｙｃｈｏｌｉｃ ａｃｉｄ，ＵＤＣＡ）对胆道梗阻肝脏部分切除（ＰＨ）后肝细胞再生的影响。方法Ｗｉｓｔａｒ大鼠随机分为正常７０％肝部分切除组（Ｎ－ＰＨ）、胆道梗阻２周７０％ＰＨ组（ＢＤＯ－ＰＨ）、ＢＤＯ—ＰＨ ＵＤＣＡ治疗组及ＢＤＯ—ＰＨ生理盐水治疗组。观察肝组织学改变，检测７０％ＰＨ后肝细胞ＢｒｄＵ标记、肝内肝细胞生长因子（ＨＧＦ）及其受体Ｍｅｔ ｍＲＮＡ表达。结果 ＵＤＣＡ治疗能促进胆道梗阻后肝功能好转并减轻肝组织学病变；ＵＤＣＡ治疗组大鼠７０％ＰＨ后肝内ＨＧＦ／Ｍｅｔ ｍＲＮＡ高峰表达值均高于ＢＤＯ—ＰＨ组（Ｐ ＜ ０．０５），肝细胞 ＢｒｄＵ高峰标记指数（５９．３９±１０．８２）％高于 ＢＤＯ—ＰＨ组肝细胞 ＢｒｄＵ高峰标记指数（３６．２２±８．３７％（ｔ＝４．１４９，Ｐ＜０．０１），而与Ｎ－ＰＮ组肝细胞ＢｒｄＵ高峰标记指数（６８．６４±１１．２６％）％相比差异无显著性（ｔ＝１．４５１，Ｐ＞０．０５）。结论 ＵＤＣＡ通过缓解胆道梗阻后肝组织损害并上调７０％ＰＨ后肝内ＨＧＦ／Ｍｅｔ ｍＲＮＡ表达，从而促进胆道梗阻肝脏部分切除后肝细胞再生。

Ursodeoxycholic acid promotes liver regeneration after partial hepatectomy in bile duct obstructive rats

OBJECTIVE: To investigate the effect of ursodeoxycholic acid (UDCA) on liver regeneration after 70% partial hepatectomy (PH) in bile duct obstructive (BDO) rats. METHODS: Wistar rats were randomly divided into N-PH group in which normal rats were operated with 70% PH, BDO-PH group in which 70% PH were operated after two week's BDO, and BDO-PH UDCA or sterile saline treatment group in which UDCA (15mg kg(-1) d(-1)) or saline was administrated during BDO and after 70% PH. The hepatic pathological changes were observed. BrdU labeling of hepatocytes, the mRNA expression of intrahepatic hepatocyte growth factor (HGF) and its receptor (Met gene) after 70% PH were measured by immunohistochemical analysis and RT-PCR, respectively. RESULTS: Improvements of hepatic function and pathological changes were induced by UDCA administration after BDO. The expression of hepatic HGF/Met mRNA after 70% PH in BDO-PH UDCA treatment group rats was significantly increased compared with N-PH group rats (P<0.05), BrdU peak labelling of hepatocytes (59.39% +/- 10.82%) in BDO-PH UDCA treatment group rats was significantly higher than that (36.22% +/- 8.37%) in BDO-PH group rats (t=4.149, P<0.01) and without significance compared with N-PH group rats (68.64% +/- 11.26%, t=1.451, P >0.05). CONCLUSIONS: UDCA promotes liver regeneration after 70% PH in BDO rats by remission of hepatic pathological changes and elevating hepatic mRNA expression of HGF and Met.