<b>背景和目的:</b>胆汁淤积是胆汁流动受限或阻塞时发生的肝脏疾病。雌激素诱导的胆汁淤积的标志是胆汁流量减少和胆汁酸在肝脏中的积累以及肝脏损伤。目的是评估蔓越莓水提取物(CWE)对EE诱导的大鼠胆汁淤积的肝保护作用。<b>材料和方法:</b>将体重约150±10g的成年白化病大鼠分为六组,每组六只动物。作为对照组,三组(I,II和IV)和三个实验组(III,V,VI).<b>结果:</b>口服CWE15天(150mgkg<sup>1</sup>b.wt.)在EE处理的大鼠中(100μgkg<sup>1</sup>5天b.wt.)改善血清胆固醇,胆汁酸和TBIL以及肝脏SOD和GPx显着。此外,CWE抑制了ALP,ALT,γ-GT活性以及TNF-α水平,NO,与EE处理大鼠相比,MMP-2和MMP-9和MDA。另一方面,与EE处理的大鼠相比,蔓越莓提取物组大鼠肝脏TLR4,NF-κB和p38MAPK基因表达下调。CWE的预防性作用II比预防性作用更明显。肝组织的组织病理学检查也支持了蔓越莓在恢复正常肝功能能力方面的保肝作用。<b>结论:</b>结果表明,蔓越莓提取物通过使TLR4、NF-κB和p38MAPK基因表达水平正常化,对EE诱导的胆汁淤积有较强的预防作用。
<b>Background and Objective:</b> Cholestasis is a liver disease that occurs when bile flow is restricted or blocked. Estrogen-induced cholestasis is marked by a reduction in bile flow and the accumulation of bile acids in the liver as well as liver damage. The aim was to evaluate the hepatoprotective effect on EE-induced cholestasis in rats of Cranberry Water Extract (CWE). <b>Materials and Methods:</b> Adult albino rats weighing approximately 150±10 g were divided into six groups of six animals each. As control groups, three groups (I, II and IV) and three experimental groups were used (III, V, VI). <b>Results:</b> Oral administration for 15 days of CWE (150 mg kg<sup>1</sup> b.wt.) in EE-treated rats (100 μg kg<sup>1</sup> 5 days b.wt.) improved serum cholesterol, bile acid and TBIL as well as hepatic SOD and GPx significantly. Also, CWE inhibited ALP, ALT, γ-GT activity as well as levels of TNF-α, NO, MMP-2 and MMP-9 and MDA in comparison with the EE treatment rats. On the other hand, the liver TLR4, NF-κB and p38MAPK gene expression was down regulated group of rats administrated with cranberry extract when compared with the EE-treated rats. CWE\'s prophylactic action II is more pronounced than prophylactic one. The hepatoprotective effects of cranberry in restoring normal liver functional ability were also supported by histopathological examination of liver tissues. <b>Conclusion:</b> The results show clearly that cranberry extract has a strong prophylactic effect in EE-induced cholestasis by normalizing the levels of TLR4, NF-κB and p38MAPK gene expression.