文献类型：期刊文献

英文题名：Inhibition of acrolein-induced autophagy and apoptosis by a glycosaminoglycan from Sepia esculenta ink in mouse Leydig cells

作者：Gu, Yi-Peng[1,2];Yang, Xiao-Mei[1];Luo, Ping[2];Li, Yan-Qun[3];Tao, Ye-Xing[4];Duan, Zhen-Hua[1];Xiao, Wei[2];Zhang, Da-Yan[4];Liu, Hua-Zhong[2]

机构：[1]Hezhou Univ, Inst Food Sci & Engn Technol, Hezhou 542899, Peoples R China;[2]Guangdong Ocean Univ, Coll Chem & Environm, 1 Haida Rd, Zhanjiang 524088, Guangdong, Peoples R China;[3]Guangdong Ocean Univ, Coll Food Sci & Technol, Zhanjiang 524088, Peoples R China;[4]Guilin Med Univ, Sci Expt Ctr, Guilin 541004, Peoples R China

年份：2017

卷号：163

起止页码：270

外文期刊名：CARBOHYDRATE POLYMERS

收录：SCI-EXPANDED(收录号：WOS:000396955500031)、、EI(收录号：20170503296341)、Scopus(收录号：2-s2.0-85010465510)、WOS

基金：This work was supported by the National Natural Science Foundation of China (Grant No. 31171667) and the Natural Science Foundation of Guangdong Province, China (Grant No. 2016A030313753).

语种：英文

外文关键词：Glycosaminoglycan; Sepia esculenta ink; Autophagy; Apoptosis; Leydig cells; Acrolein

外文摘要：In our recent reports, a squid ink polysaccharide (SIP) was found having preventive activity against cyclophosphamide induced damage in mouse testis and ovary. Here we further reveal the regulative mechanism of SIP against chemical toxicity on testis. Leydig cells exposed to acrolein (ACR) underwent apoptosis at 12 h and 24 h. Before apoptosis, cells occurred autophagy that was confirmed by high autophagic rate and Beclin-1 protein content at 3 h. PI3K/Akt and p38 MAPK signal pathways involved in the regulatory mechanisms. These outcomes of ACR were recovered completely by SIP, which was demonstrated by attenuated disruption of redox equilibrium and increased testosterone production, through suppressing ACR-caused autophagy and apoptosis regulated by PI3K/Akt and p38 MAPK signal pathways in Leydig cells. Summarily, autophagy occurred before apoptosis caused by ACR-activated p38 MAPK and PI3K/Akt pathways were blocked by SIP, resulting in survival and functional maintenance of Leydig cells. (C) 2017 Elsevier Ltd. All rights reserved.