绿原酸保护由脂多糖诱导引起的大鼠慢性肝脏损伤

本文采用脂多糖诱导建立大鼠慢性肝脏损伤模型,研究了绿原酸对大鼠慢性肝脏损伤的保护作用。将成年SD大鼠随机分LPS模型组和绿原酸干预组,实验持续28 d后进行取样。记录大鼠的生长性能和肝脏重量,并计算肝脏指数;检测血清中谷丙转氨酶(ALT)、谷草转氨酶(AST)、碱性磷酸酶(ALP)活性和总胆红素(TBIL)、总蛋白(TP)含量;HE染色观察肝组织病理变化;检测肝脏组织中超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量。结果表明,绿原酸能够显著降低慢性肝脏损伤大鼠的末重、平均日增重和食物转化率(P0.05);显著降低大鼠肝脏重量和肝脏指数(P0.05);显著降低血清中ALT、AST、ALP活性和TBIL含量(P0.05或P0.01),降幅分别为12%、13%、17%和50%;显著升高血清中TP含量和肝脏组织中SOD活性(P0.01或P0.05),增幅分别为17%和23%;显著降低肝脏组织中MDA含量(P0.05),降幅为33%;绿原酸能够改善慢性肝脏损伤大鼠的肝组织结构。因此,绿原酸对长期脂多糖应激引起的大鼠慢性肝脏损伤有一定的保护作用。

Protective Effects of Chlorogenic Acid on Lipopolysaccharide-induced Chronic Liver Injury in Rats

Rats were randomly divided into the model group and chlorogenic aid (CGA)-supplemented group, and at the 28th day the rats were sacrificed. The growth performance, liver weight and liver index of each rat were analyzed. The activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) and the contents of total bilirubin (TBIL) and total protein (TP) in serum were assayed. Hepatic pathological changes were observed by H&E staining method. The activities of superoxide dismutase (SOD) and the malondialdehyde (MDA) content in liver were determined. Compared with the model group, the finish body weight, average daily gain and food efficiency ratio (FER), liver weight and liver?index in CGA-supplemented group were significantly decreased (P<0.05). The activities of ALT, AST, ALP and the level of TBIL in serum declined significantly (P<0.05 or P<0.01), and the declining rates were 12%, 13%, 17% and 50%, respectively. TP content in serum and SOD activity in liver were significantly increased (P<0.01 or P<0.05), and the increasing rate was 17% and 23%, respectively. MDA content in liver declined significantly (P<0.05), and the declining rate was 33%. H&E staining indicated that the hepatic pathological injury in CGA-supplemented group was attenuated. Therefore, CGA has a protective effect on chronic liver injury induced by lipopolysaccharide.