熊去氧胆酸对他莫昔芬所致Wistar大鼠肝毒性的治疗作用

Elias Adikwu, B. Bokolo
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引用次数: 0

摘要

背景。临床使用他莫昔芬(TAM)可能引起肝毒性。熊去氧胆酸(UDCA)具有良好的肝脏保护作用。本研究评估了UDCA对tam诱导的大鼠肝毒性的保护作用。材料和方法。35只成年雌性Wistar大鼠,每组7只,n=5只。给药10 d:第1组:水(10 mL/kg/d;安慰剂对照)每次口服[p。0],第二组:乙醇1% (1mL/kg/天;第3组:UDCA (40 mg/kg/day/p.o),第4组:TAM (45 mg/kg/day) i.p。第5 ~ 7组分别用UDCA(10、20、40 mg/kg)预处理,然后再用TAM (45 mg/kg/day) i.p。第11天,采集血液样本并评估血清肝脏生物标志物。肝脏样本进行氧化应激标志物和组织学评估。与安慰剂对照组相比,TAM治疗组大鼠体重显著(p<0.05)降低,肝脏重量显著(p<0.01)增加。与对照组相比,TAM显著(p<0.001)提高了血清碱性磷酸酶、乳酸脱氢酶、γ -谷氨酰转移酶、转氨酶、胆红素、高密度脂蛋白胆固醇水平和肝脏丙二醛水平。与对照组相比,TAM显著(p<0.001)降低了肝脏谷胱甘肽、过氧化氢酶、谷胱甘肽过氧化物酶、超氧化物歧化酶、血清总蛋白、白蛋白总胆固醇、低密度脂蛋白胆固醇和甘油三酯水平。tam处理的大鼠出现脂肪变性和坏死改变。与TAM相比,UDCA预处理显著阻止TAM诱导的血清生化指标和氧化应激指标的变化,且呈剂量相关。UDCA可预防tam诱导的肝组织改变。UDCA可能在临床上对TAM相关的肝毒性有效。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Therapeutic benefit of ursodeoxycholic acid in tamoxifen-induced hepatotoxicity in Wistar rats
Background. The clinical use of tamoxifen (TAM) may cause hepatotoxicity. Ursodeoxycholic acid (UDCA) has promising liver protective activity. This study assessed the protective effect of UDCA on TAM-induced hepatotoxicity in rats.Material and methods. Thirty five adult female Wistar rats were grouped into 7 of n=5/group. The rats were treated for 10 days as follows: Group 1: Water (10 mL/kg/day; placebo control) per oral [p.o], group 2: Ethanol 1% (1mL/kg/day; vehicle control) intraperitoneally (i.p), group 3: UDCA (40 mg/kg/day/p.o) and group 4: TAM (45 mg/kg/day) i.p. Groups 5-7 were pretreated with UDCA (10, 20 and 40 mg/kg), before daily treatment with TAM (45 mg/kg/day) i.p, respectively. On day 11, blood samples were collected and assessed for serum liver biomarkers. Liver samples were evaluated for oxidative stress markers and histology.Results. Significantly (p<0.05) decreased body weight and significantly (p<0.01) increased liver weight occurred in TAM- treated rats when compared to placebo control. TAM significantly (p<0.001) increased serum alkaline phosphatase, lactate dehydrogenase, gamma-glutamyl transferase, aminotransferases, bilirubin, high density lipoprotein cholesterol levels and liver malondialdehyde levels when compared to control. TAM significantly (p<0.001) decreased liver glutathione, catalase, glutathione peroxidase, superoxide dismutase, serum total protein, albumin total cholesterol, low density lipoprotein cholesterol and triglyceride levels when compared to control. Steatosis and necrotic changes occurred in TAM-treated rats. UDCA pretreatment significantly prevents TAM-induced changes in serum biochemical markers, and oxidative stress indices in a dose-related fashion when compared to TAM. UDCA prevents TAM-induced changes in liver histology.Conclusion. UDCA may be clinically effective for TAM associated hepatotoxicity.
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