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纸质出版日期:2016
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徐亚沙, 吴芹, 熊庭旺, 等. 清胰Ⅱ号对小鼠胆汁淤积性肝损伤的保护作用[J]. 中国实验方剂学杂志, 2016,22(8):166-170.
XU Ya-sha, WU Qin, XIONG Ting-wang, et al. Protective Effect of Qingyi II on BDL-Induced Cholestatic Liver Injury in Mice[J]. Chinese journal of experimental traditional medical formulae, 2016, 22(8): 166-170.
徐亚沙, 吴芹, 熊庭旺, 等. 清胰Ⅱ号对小鼠胆汁淤积性肝损伤的保护作用[J]. 中国实验方剂学杂志, 2016,22(8):166-170. DOI: 10.13422/j.cnki.syfjx.2016080166.
XU Ya-sha, WU Qin, XIONG Ting-wang, et al. Protective Effect of Qingyi II on BDL-Induced Cholestatic Liver Injury in Mice[J]. Chinese journal of experimental traditional medical formulae, 2016, 22(8): 166-170. DOI: 10.13422/j.cnki.syfjx.2016080166.
目的: 本研究旨在探讨清胰Ⅱ号对胆管结扎造成的胆汁淤积性肝损伤的保护作用及其机制。方法: 昆明种小鼠随机分为假手术组
模型组
低、高剂量清胰Ⅱ号组(0.5
1.0 g·kg-1)
连续ig给药7 d后
采用胆管结扎(BDL)术制备小鼠肝脏胆汁淤积性肝损伤模型
制模后72 h麻醉处死动物
收集血液和肝脏观察各组生化指标和肝组织病理学改变以及实时荧光定量-聚合酶链式反应(qPCR)检测肝脏胆酸代谢通路相关基因的mRNA水平的表达。结果: 与假手术组比较
模型组丙氨酸氨基转移酶(ALT)
碱性磷酸酶(ALP)
总胆汁酸(TBA)
总胆红素(TBIL)水平均显著增高
肝组织病理显示在大量中性粒细胞浸润、肝细胞水肿、变性和坏死
同时胆酸合成基因胆固醇7α-羟化酶(Cyp7a1)
甾醇12α-羟化酶(Cyp8b1)
类法尼酯衍生物X受体(FXR)
小分子异源二聚体伴侣(SHP)
牛磺胆酸钠协同转运蛋白(Ntcp) mRNA表达均降低(P<0.05);与模型组比较
给药组可降低ALT
ALP活性和TBA
TBIL水平
改善其病理损伤
上调上述基因mRNA水平(P<0.05)。结论: 清胰Ⅱ号对胆汁淤积性肝损伤具有保护作用
通过作用于肝脏中与胆汁酸合成和转运相关的基因表达
以维持胆汁酸的稳态。
Objective: To investigate the protective effect of QingyiⅡ (QY) on the bile-duct ligation (BDL)-induced cholestatic liver injury. Method: Kunming mice were randomly divided into the sham operation group
model group
QY-0.5 group (0.5 g·kg-1) and QY-1.0 group (1.0 g·kg-1)
and orally administered for 7 days. On the 7th day
mice received BDL to prepare the cholestatic liver injury model. Livers and blood were collected 72 hours later after BDL. Serum enzyme biochemical indexes
histopathological changes and genes expression were determined. Result: Compared with sham operation group
there were significant increases in serum alanine aminotransferase (ALT) and alkaline phosphatase (ALP)
increased total bile acid (TBA) and total bilirubin (TBIL) in model group. According to hepatic tissue pathological indexes
neutrophile infiltration and hepatocyte necrosis were apparent
the expression of cholesterol-7α-hydroxylase (Cyp7a1)
12α-hydroxylase (Cyp8b1)
farnesoid X receptor (FXR)
small heterodimer partner (SHP) and Ntcp mRNA expression were decreased (P<0.05). Compared with model group
QY decreased ALT
ALP activities and TBA
TBIL levels
alleviated the pathological injury
and up-regulated the expression of above genes (P<0.05). Conclusion: QY II could protect against cholestatic liver injury
and maintain the stability of bile acid by regulating gene expressions related to bile acid synthesis and transport in liver.
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