目的 研究胡黃連苷Ⅱ?qū)λ穆然迹–Cl₄）誘導(dǎo)的大鼠急性肝損傷的保肝和利膽作用。方法 保肝作用和利膽作用研究各選取60只健康SD大鼠，均隨機(jī)分為6組：對(duì)照組、模型組、溶劑對(duì)照組和胡黃連苷II低、中、高劑量（2.5、5.0、10.0 mg·kg^-1）組，除對(duì)照組外，其余5組大鼠分別1次性ip給予CCl₄油溶液（50%橄欖油、2 mL·kg^-1）制備急性肝損傷模型。保肝作用研究：在造模后3、24和48 h ig給藥1次，對(duì)照組和模型組ig給予等體積生理鹽水，溶劑對(duì)照組ig給予等體積溶劑，試劑盒法檢測(cè)血清中丙氨酸氨基轉(zhuǎn)移酶（ALT）、天氨酸氨基轉(zhuǎn)移酶（AST）、堿性磷酸酶（ALP）、總膽紅素（TBIL）、總膽汁酸（TBA）、腫瘤壞死因子-α （TNF-α）、白細(xì)胞介素-8 （IL-8）及白細(xì)胞介素-6 （IL-6）水平和肝組織中丙二醛（MDA）、超氧化物歧化酶（SOD）、過氧化氫酶（CAT）、谷胱甘肽S轉(zhuǎn)移酶（GST）、谷胱甘肽（GSH）及谷胱甘肽過氧化物酶（GSH-Px）水平； HE染色觀察肝組織病理改變。利膽作用研究：大鼠造模12 h之后進(jìn)行膽管插管，并通過十二指腸給藥，給藥前及給藥后30、60、90及120 min分別記錄膽汁流量。結(jié)果 與模型組比較，胡黃連苷II能顯著降低血清中肝功能生化指標(biāo)ALT、AST、ALP、TBA和TBIL水平（P<0.01）；顯著降低大鼠肝臟MDA水平，并顯著增加肝臟SOD、CAT、GSH、GST及GSH-Px水平（P<0.01）；顯著降低血清TNF-α、IL-6及IL-8水平（P<0.01），且呈劑量相關(guān)性。胡黃連苷II各劑量均可不同程度減輕模型大鼠肝臟病變范圍與程度。與模型組比較，各給藥后時(shí)間點(diǎn)胡黃連苷II均可顯著增加膽汁流量（P<0.01），且呈劑量相關(guān)性。結(jié)論 胡黃連苷II能顯著緩解CCl₄誘導(dǎo)的大鼠急性肝損傷并增加膽汁流量。

Objective To study the hepatoprotective and choleretic effects of picroside II on carbon tetrachloride (CCl₄) -induced acute liver injury in rats. Methods Sixty healthy SD rats were selected respectively for liver protection and cholagogic effects, and were randomly divided into six groups respectively:control group, model group, solvent control group and picroside II low-dose, medium-dose and high-dose (2.5, 5.0, 10.0 mg·kg^-1) groups. Except for the control group, rats were given CCl₄ oil solution (50% olive oil, 2 mL·kg^-1) by ip once to prepare acute liver injury model. Study on liver protection:The drug was administered once at 3, 24 and 48 h after modeling, control group and model group were ig given equal volume of normal saline, and solvent control group was ig given equal volume of solvent. The levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total bilirubin (TBIL), total bile acid (TBA), tumor necrosis factor- α (TNF- α), interleukin-8 (IL-8) and interleukin-6 (IL-6) in serum and malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione S transferase (GST), glutathione (GSH) and glutathione peroxidase (GSH-Px) in liver tissues were detected by kit method. HE staining was used to observe the pathological changes of liver tissue. Cholagogic effect study:Bile duct intubation was performed 12 h after rat modeling, and bile flow was recorded before and 30, 60, 90 and 120 min after administration. Results Compared with model group, picroside Ⅱ could significantly reduce the levels of ALT, AST, ALP, TBA and TBIL in serum (P<0.01), increased the levels of SOD, CAT, GSH, GST and GSH-Px in liver significantly (P<0.01), significantly decreased serum TNF-α, IL-6 and IL-8 levels (P<0.01), in a dose-dependent manner. The range and degree of liver lesions in model rats could be alleviated by different doses of picroside Ⅱ. Compared with model group, picroside Ⅱ significantly increased bile flow at time points after administration (P<0.01), in a dose-dependent manner. Conclusion Picroside II could alleviate CCl₄-induced acute liver injury and cholestasis in rats.

R285.5