文献类型：期刊文献

英文题名：Inhibition of chemotherapy-induced apoptosis of testicular cells by squid ink polysaccharide

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

机构：[1]Hezhou Univ, Inst Food Res, Hezhou 542899, Guangxi, Peoples R China;[2]Guangdong Ocean Univ, Dept Appl Chem, Coll Chem & Environm, 1 Sea Rd, Zhanjiang, Guangdong 524088, Peoples R China;[3]Chinese Acad Agr Sci, Guangxi Buffalo Res Inst, Nanning 530001, Guangxi, Peoples R China

年份：2017

卷号：14

期号：6

起止页码：5889

外文期刊名：EXPERIMENTAL AND THERAPEUTIC MEDICINE

收录：SCI-EXPANDED(收录号：WOS:000417815000093)、、Scopus(收录号：2-s2.0-85032572887)、WOS

基金：This study was supported by the National Natural Science Foundation of China (grant no. 31171667), the Special Fund for Distinguished Experts in Guangxi and the Guangxi Talent Highland of Preservation and Deep Processing Research in Fruit and Vegetables.

语种：英文

外文关键词：squid ink polysaccharide; cyclophosphamide; testicular germ cells; apoptosis

外文摘要：The aim of this study was to determine the mechanisms driving the protective effects of squid ink polysaccharide (SIP) against cyclophosphamide (CP)-induced testicular damage, focusing on germ cells. In the testes of mice exposed to CP and/or SIP, the present study examined the levels of reactive oxygen species (ROS) and malondialdehyde, activity of superoxide dismutase levels, protein expression levels of B-cell lymphoma 2 (Bcl2), Bcl2-associated X protein (Bax), and total Caspase 3, activation of p-p38 and p-Akt proteins, and tissue morphology. The findings indicated that CP induced ROS production and oxidative stress, resulting in testicular damage. However, under administration of SIP, oxidative stress was impaired and the testicular toxicity induced by CP was weakened, which implied that SIP may have an important role in preventing chemotherapeutic damage to the male reproductive system via promoting antioxidant ability. Furthermore, the altered expression levels, including the upregulation of Bax and Caspase 3, downregulation of Bcl-2 and the increased Bax/Bcl-2 ratio, indicated that apoptosis occurred in CP exposed testes of mice; however, the alterations were reversed in mice treated with SIP. Moreover, in CP-exposed testes, p38 and Akt proteins were significantly phosphorylated (P<0.05), whereas in the testes of mice co-treated with SIP and CP, phosphorylation of the two proteins was inhibited, demonstrating that the two signalling pathways participated in the regulative processes of the deleterious effects caused by CP, and the preventive effects SIP mediated.