目的 考察胡黃連苷Ⅱ（PSⅡ）對(duì)大鼠膽管結(jié)扎膽汁淤積模型的改善作用。方法 采用膽總管結(jié)扎建立大鼠膽汁淤積模型，另取10只大鼠只分離膽管不結(jié)扎，作為假手術(shù)組（0.5% CMC-Na），50只膽管結(jié)扎大鼠隨機(jī)分為5組：模型組（0.5% CMC-Na）、熊去氧膽酸（UCDA）100 mg/kg陽性藥組和PSⅡ 80、40和20 mg/kg組，造模后各組連續(xù)ig給藥7 d。觀察大鼠一般狀況及體質(zhì)量；試劑盒法檢測(cè)血清丙氨酸轉(zhuǎn)氨酶（ALT）、天冬氨酸轉(zhuǎn)氨酶（AST）、白蛋白（ALB）、堿性磷酸酶（ALP）、谷氨酰轉(zhuǎn)肽酶（GGT）、總膽紅素（TBIL）、總膽汁酸（TBA）水平；取肝臟稱質(zhì)量，計(jì)算肝臟系數(shù)；試劑盒法測(cè)定肝臟組織勻漿中超氧化物歧化酶（SOD）、過氧化氫酶（CAT）、谷胱甘肽過氧化物酶（GSH-Px）活性，勻漿上清液中髓過氧化物酶（MPO）活性。結(jié)果 與模型組比較，PSⅡ?qū)δＰ痛笫笠话銧顟B(tài)和體質(zhì)量無明顯影響，可顯著降低模型大鼠肝臟系數(shù)（P<0.01、0.05）；PSⅡ 80、40 mg/kg給藥均可顯著降低模型大鼠血清ALT、AST、ALP、GGT、TBIL水平，80 mg/kg對(duì)血清TBA也發(fā)揮顯著降低作用（P<0.01）；PSⅡ 80、40 mg/kg給藥均可顯著升高肝臟SOD和CAT活性（P<0.05、0.01），對(duì)肝臟GSH-Px活性未見明顯影響，均可顯著降低肝臟MPO活性（P<0.05、0.01）。結(jié)論 PSⅡ?qū)τ诖笫竽懝芙Y(jié)扎所致的膽汁淤積性肝損傷具有明顯的改善作用，涉及的機(jī)制可能包括上調(diào)肝組織抗氧化酶活性及抑制炎性細(xì)胞活化和浸潤。

Objective To investigate the effect of picroside Ⅱ (PSⅡ) on the cholestasis of bile duct ligation in rats. Methods Cholestasis model was established by common bile duct ligation, another 10 rats were separated from the bile duct without any ligature as the sham operation group (0.5% CMC-Na). Fifty rats with bile duct ligation were randomly divided into five groups:model group (0.5% CMC-Na), UCDA (100 mg/kg, positive drug) group, PSⅡ 80, 40 and 20 mg/kg group. After modeling, rats in each group were ig administered continuously for 7 days. The general condition and body weight of rats were observed. The levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), albumin (ALB), alkaline phosphatase (ALP), glutamyl transpeptidase (GGT), total bilirubin (TBIL) and total bile acid (TBA) were measured by kit method. The liver weight was taken to calculate the liver coefficient, and the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) in liver homogenate and myeloperoxidase (MPO) in the supernatant of liver homogenate were determined by kit method. Results Compared with the model group, PSⅡ had no significant effect on the general state and body weight of the model rats, but could significantly reduce the liver coefficient of the model rats (P<0.01, 0.05); The serum levels of ALT, AST, ALP, GGT, and TBIL in model rats were significantly decreased after 80 and 40 mg/kg PSⅡ administration, and serum TBA was also significantly reduced by 80 mg/kg (P<0.01). PSII 80 and 40 mg/kg administration could significantly increase the activity of SOD and CAT in liver, but there was no significant difference in liver GSH-Px activity,and both 80 and 40 mg/kg PSII administration significantly reduced liver MPO activity (P<0.01, 0.05).Conclusion PSII can significantly improve cholestatic liver injury caused by bile duct ligation in rats.The mechanisms involved may include up-regulating the activity of antioxidant enzymes in liver and inhibiting activation and infiltration of inflammatory cells.