中文摘要：

目的：初步探讨Colgalt2基因介导的胶原Glcα1，2 Galβ1？糖基化修饰在急性肝损伤过程中的作用。方法取60只Colgalt2＋／＋小鼠和60只Colgalt2－／－小鼠进行急性肝损伤实验，雌雄各半。每组随机选取20只小鼠腹腔注射CCl4（CCl4∶橄榄油＝2∶7，20 ml／kg）。观察小鼠死亡情况，并绘制生存曲线。每组剩余40只小鼠随机分为0、4、8、12 h组，每组10只，腹腔注射CCl4（剂量同上）。分别于0、4及8 h各处死6只小鼠，之后将4及8 h组剩余的小鼠均纳入12 h组（ Colgalt2＋／＋小鼠， n＝14； Colgalt2－／－小鼠， n＝16），并于12 h处死小鼠。 HE染色观察肝组织的病理学改变，取血清进行生化指标ALT、 AST测定。利用qRT？PCR和Western印迹技术检测小鼠Colgalt2在基因及蛋白水平的表达情况。结果Colgalt2基因在Col？galt2＋／＋小鼠肝组织内表达，而在Colgalt2－／－小鼠肝组织内不表达。注射CCl4后10 h， Colgalt2＋／＋小鼠死亡率为35％， Colgalt2－／－小鼠死亡率为70％，两组小鼠死亡率差异显著（P＜0．05）。注射CCl4后12 h， Colgalt2＋／＋小鼠死亡率达50％， Colgalt2－／－小鼠死亡率为70％，差异不显著（P＞0．05）。肝功检测及HE染色结果均提示，与Colgalt2＋／＋小鼠相比， Colgalt2－／－小鼠肝损伤较重。注射CCl4后，野生型小鼠Colgalt2在RNA水平和蛋白水平表达下调。结论 Colgalt2基因敲除在一定程度上可加重小鼠急性肝损伤。该观察结果提示， Colgalt2基因介导的胶原Glcα1，2 Galβ1？糖基化修饰可能与肝损伤的修复有关。

英文摘要：

Objective To investigate the role of Colgalt2-mediated collagen Glcα1 , 2 Galβ1-glycosylation in CCl4-induced acute liver injury. Methods The C57 BL/6 J mice were divided into two groups： Colgalt2 ＋/ ＋mice （ n=60 ） and Colgalt2 -/ - mice （ n=60 ） , half male and half fe-male. Twenty mice were randomly selected from each group and intraperitoneally injected with CCl4 solution （CCl4∶oil 2∶7 （v/v）, 20 ml/kg body weight） . The deaths of mice were recorded and＆amp;nbsp;the survival curve drawn. Additionally, the rest of mice in each group were divided into four groups：0 h, 4 h, 8 h, 12 h groups, 10 mice in each group. They were treated with CCl4 as mentioned a-bove. Six mice were sacrificed at each time point. The rest mice in 4 h group and 8 h group were brought into 12 h group （ Colgalt2 ＋/ ＋ mice group, n =14; Colgalt2 -/ - mice group, n =16 ） . Then, all mice were sacrificed at 12 h. The expression of Colgalt2 gene in mice was detected by Western blotting and qRT-PCR. Serum AST and ALT levels were determined and liver tissues of the mice were examined by HE staining. Results Colgalt2 gene was expressed in the liver tissues of Colgalt2 ＋/ ＋ mice but not in Colgalt2 -/ - mice. The mortality of Colgalt2 ＋/ ＋ mice was 35% and that of Colgalt2 -/ - mice was 70 % at 10 h after injection of CCl4 and the difference was significant （ P〈0. 05） . At 12 h, the mortality of Colgalt2 ＋/ ＋ mice was 50 %, which was not significantly dif-ferent from that of Colgalt2 -/ - mice （ 70 %） （ P〉0. 05 ） . Liver function test and HE staining showed that liver injury in Colgalt2 -/ - mice was severer than that in Colgalt2 ＋/ ＋ mice. Colgalt2 at the level of RNA and protein was down-regulated after injection of CCl4. Conclusion Colgalt2 gene knock-out may aggravate the liver injury of mice to some extent. Collagen Glcα1 , 2 Galβ1-glycosy-lation mediated by Colgalt2 may be related to the repair of liver injury.