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目的研究巴西莓对大鼠慢性酒精性肝损伤的保护作用及机制。方法Wistar大鼠适应性喂养一周后随机分为空白对照组、模型组、阳性药对照组和巴西莓1.6、0.8、0.4 g/kg BW 3个剂量组,除空白组给蒸馏水外,其余各组均用56%白酒灌胃,剂量为第一周0.8 ml/100g,以后每周增加0.1 ml(直至增加为1.5 ml/100g),连续灌胃8周,建立大鼠慢性酒精性肝损伤模型。HE染色观察巴西莓冻干粉对慢性酒精性肝损伤大鼠肝细胞病理改变的影响,放射免疫分析法测定血清转化生长因子-β1(TGF-β1)含量,RT-PCR测定肝脏组织TGF-β1、分化抗原簇-68(CD68)mRNA表达,免疫组化法测定肝脏CD68蛋白表达。结果病理切片观察表明模型组肝脏以脂肪变性为主,部分肝脏可见肝细胞点状坏死,炎性细胞浸润,阳性药及巴西莓各剂量对大鼠肝脏病理改变有不同程度的改善作用。巴西莓可以降低血清TGF-β1含量(P<0.01),降低肝脏TGF-βmRNA表达(P<0.05),降低肝脏CD-68 mRNA(P<0.01)及蛋白表达(P<0.01)。结论巴西莓对酒精性肝损伤具有一定的保护作用,其机制可能与抑制TGF-β1、CD68表达有关。
Objective To study the protective effect and mechanism of Acai berry on chronic alcoholic liver injury in rats. Methods One week after the adaptive feeding, Wistar rats were randomly divided into three groups: blank control group, model group, positive control group and Acremonium citriclum 1.6,0.8,0.4 g / kg BW. Except the control group, All rats were given gastric perfusion with 56% alcohol at the dosage of 0.8 ml / 100g for the first week and 0.1 ml / week for the first week (up to 1.5 ml / 100g). The model was established by chronic alcoholic liver injury in rats. HE staining was used to observe the effect of Lycium barbarum lyophilized powder on pathological changes of liver cells in rats with chronic alcoholic liver injury. The content of TGF-β1 was measured by radioimmunoassay. The expression of TGF-β1 , Differentiation of antigen cluster -68 (CD68) mRNA expression, liver CD68 protein expression by immunohistochemistry. Results The pathological sections showed that the liver of the model group was mainly of steatosis. Some of the liver showed punctate necrosis of hepatocytes, inflammatory cell infiltration, positive drug and each dose of Acai berry on liver pathological changes in rats to varying degrees. Acai berry could decrease the content of TGF-β1 in serum, decrease the expression of TGF-βmRNA in liver and decrease the expression of CD-68 mRNA and protein in liver (P <0.01). Conclusion Acai berry has a protective effect on alcoholic liver injury, which may be related to the inhibition of the expression of TGF-β1 and CD68.