肝脏再生增强因子（ALR）抑制刀豆蛋白A诱导的小鼠肝炎。
Augmenter of liver regeneration (ALR) restrains concanavalin A-induced hepatitis in mice.
作者信息
Mu Mao, Zhang Zhenwei, Cheng Yi, Liu Guangze, Chen Xiusheng, Wu Xin, Zhuang Caifang, Liu Bingying, Kong Xiangping, You Song
机构信息
School of Life Science and Biopharmaceutical Sciences, Shenyang Pharmaceutical University, 103 Wenhua Road, Shenyang 110016, People's Republic of China; Liver Disease Key Laboratory, Center of Infectious Diseases, 458 Hospital, 801 Dongfengdong Road, Guangzhou 510600, People's Republic of China.
Liver Disease Key Laboratory, Center of Infectious Diseases, 458 Hospital, 801 Dongfengdong Road, Guangzhou 510600, People's Republic of China.
出版信息
Int Immunopharmacol. 2016 Jun;35:280-286. doi: 10.1016/j.intimp.2016.03.040. Epub 2016 Apr 16.
Augmenter of liver regeneration (ALR), produced and released by hepatocytes, has cytoprotective and immunoregulatory effects on liver injury, and has been used in many experimental applications. However, little attention has been paid to the effects of ALR on concanavalin A (Con A)-induced hepatitis. The purpose of this paper is to explore the protective effect of ALR on Con A-induced hepatitis and elucidate potential mechanisms. We found that the ALR pretreatment evidently reduced the amount of ALT and AST in serum. In addition, pro-inflammatory cytokines, chemokines and iNOS were suppressed. ALR pretreatment also decreased CD4(+), CD8(+) T cell infiltration in liver. Besides, we observed that ALR pretreatment was capable of suppressing the activation of several signaling pathways in Con A-induced hepatitis. These findings suggest that ALR can obviously weaken Con A-induced hepatitis and ALR has some certain immune regulation function.
肝脏再生增强因子（ALR）由肝细胞产生并释放，对肝损伤具有细胞保护和免疫调节作用，已被用于许多实验应用中。然而，人们对ALR对刀豆蛋白A（Con A）诱导的肝炎的影响关注甚少。本文旨在探讨ALR对Con A诱导的肝炎的保护作用，并阐明其潜在机制。我们发现，ALR预处理明显降低了血清中ALT和AST的含量。此外，促炎细胞因子、趋化因子和诱导型一氧化氮合酶（iNOS）受到抑制。ALR预处理还减少了肝脏中CD4(+)、CD8(+) T细胞浸润。此外，我们观察到ALR预处理能够抑制Con A诱导的肝炎中几种信号通路的激活。这些发现表明，ALR可以明显减轻Con A诱导的肝炎，并且ALR具有一定的免疫调节功能。
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