Squid ink polysaccharide prevents autophagy and oxidative stress affected by cyclophosphamide in Leydig cells of mice: a pilot study
文献类型: 外文期刊
第一作者: Gu, Yi-Peng
作者: Gu, Yi-Peng;Yang, Xiao-Mei;Duan, Zhen-Hua;Gu, Yi-Peng;Luo, Ping;Liu, Hua-Zhong;Gu, Yi-Peng;Xiao, Wei;Zhang, Da-Yan;Shang, Jiang-Hua
作者机构:
关键词: Autophagy;Cyclophosphamide;Leydig cells;Oxidative stress;Squid ink polysaccharide
期刊名称:IRANIAN JOURNAL OF BASIC MEDICAL SCIENCES ( 影响因子:2.699; 五年影响因子:2.629 )
ISSN: 2008-3866
年卷期: 2017 年 20 卷 11 期
页码:
收录情况: SCI
摘要: Objective(s): The aim of this study was to explore the effects of Squid ink polysaccharide (SIP) on prevention of autophagy and oxidative stress induced by cyclophosphamide (CP) in Leydig cells of mice. Materials and Methods: Examination of reproductive organ exponents, abnormal sperm rate, activities of superoxide dismutase (SOD), catalase (CAT), contents of malondialdehyde (MDA), and histological structure were performed to detect the optimal dose of SIP against oxidative stress damage in vivo, and autophagyassociated protein LC3 and Beclin-1 were examined by immunofluorescence, and their expression was detected by Western blot analysis. Leydig cells ultrastructural changes were observed by transmission fluorescent microscope. Results: SIP significantly inhibited sperm aberration, histological structure and injury of seminiferous tubules caused by CP, as well as the antioxidant activity of SOD and CAT were increased; contents of MDA were decreased. The optimal dose of SIP for prevention of oxidative stress injury by CP was 80 mg/kg. In addition, LC3 and Beclin-1 fluorescent granules were much less in the Leydig cell layer after treatment via SIP compared with the CP-treated group, and the expression levels of LC3 and Beclin-1 were also decreased. Furthermore, characteristics of cell autophagy such as mitochondrial swelling, autophagic vacuoles, and chromatin pyknosis were observed in CP-treated Leydig cells, but SIP could effectively weaken injury of Leydig cell ultrastructure by CP. Conclusion: SIP, as an antioxidant, prevents the cytoskeleton damage through up-regulation antioxidant capacity and inhibition autophagy caused by CP.
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