大鲵低聚糖肽对四氯化碳致小鼠急性肝损伤的保护作用

Hepatoprotective effects of Giant salamander glycopeptides against carbon tetrachloride(CCl_4)-induced hepatic injury in mice

研究大鲵低聚糖肽(GSGPs)对小鼠CCl4急性肝损伤的保护作用。经腹腔注射CCl4制备小鼠急性肝损伤模型,分别灌胃三种不同浓度的GSGPs,以联苯双酯(200mg(/kg·d))作为阳性对照。检测血清中谷草转氨酶(AST)、谷丙转氨酶(ALT)活性,肝组织中丙二醛(MDA)含量,超氧化物岐化酶(SOD)活性,观察小鼠肝组织形态学变化。结果表明:GSGPs中(400mg(/kg·d))、高(800mg(/kg·d))剂量组可显著抑制小鼠肝脏组织中由CCl4造成的血清中AST、ALT活性的升高,明显降低肝组织MDA含量,并且提高肝组织中SOD活性。光镜检查结果表明,CCl4模型组肝细胞明显肿胀变形,肝细胞索紊乱,伴有炎症细胞侵润。GSGPs各剂量组的肝细胞索排列整齐、肝细胞排列规则,较模型组肝组织损伤明显减轻。说明GSGPs具有保护CCl4急性肝损伤的作用。

The present study aimed at evaluating the hepatoprotective effects of GSGPs （Giant Salamander glycopeptides） on the carbon tetrachloride（CCl4） -induced hepatic injury in mice. CCI4 was administered intraperitoneally （IP） to establish the CCI4-induced acute liver injury mouse model. These mice were simultaneously given by gavage using three different doses of GSGPs （prepared from Andrias davidianus mucus by enzymatic hydrolysis）. The positive control was administrated with 200mg/kg biphenyl dimethyl dicarboxylate （DDB）. Aspartate transaminase （AST） and alanine transaminase （ALT） levels in serum,as well as malondialdehyde （MDA） content and superoxide dismutase （SOD） activity in liver were measured. Histomorphology changes in liver tissues were evaluated by the optical microscope. Results showed：acute hepatic injury protections of GSGPs were demonstrated by the fact that increases in activity of liver AST and ALT caused by CCl4 in mice treated with middle （400mg/（kg.d）） and high （800mg/（kg.d）） doses of GSGPs were significantly inhibited while the MDA content was significantly lowered and SOD activity enhanced as well. Microscopic observations showed that in the CCI4 model group,liver cells were markedly swelled and deformed with inordinate liver cell cords and accompanied inflammatory cell infiltration. However,in the liver of mice treated with low,middle and high concentrations of GSGPs,liver cell cords were arranged in order,liver cells were regular arranged ,and the damage was significantly reduced compared with the model group. Results indicated that CCl4 acute liver damages could be inhibited by GSGPs.