期刊
CARBOHYDRATE POLYMERS
卷 186, 期 -, 页码 321-331出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.carbpol.2018.01.075
关键词
Polysaccharide; Ostrea rivularis; Reproductive oxidative stress damage; Keap1-Nrf2/ARE pathway
资金
- National Natural Science Foundation of China [81503387]
- Natural Science Fund for Colleges and Universities in Jiangsu Province of China [15KJB360002]
- Six Talent Peaks Project in Jiangsu Province [2015-XCL-036, 2017-YY-003]
- Qing Lan Project of Jiangsu Province, Guangdong Provincial Science and Technology Program - Basic Conditions for Construction of Science and Technology Projects [2014A030304059]
- Application Science and Technology Research Special Program of Guangdong [2015B020234008]
- Open Funds of Jiangsu Key Laboratory of Special Resource Development and Medical Research [LPRK201704]
- construction of high level university in Guangzhou University of Chinese Medicine [A1-AFD018161Z1521]
The purpose of this study was to investigate the effects of Ostrea rivularis polysaccharide (ORP) against testicular oxidative stress injury via kelch-like ECH-associated protein 1-nuclear erythroid 2-related factor 2/antioxidant response element (Keap1-Nrf2/ARE) pathway. In pharmacological experiments in vivo, ORP administration could dose-dependently inhibit body and testicular weight loss, ameliorate epididymal sperm quality and protect reproductive impairment in cyclophosphamide-induced male Balb/c mice. Moreover, the mechanism in vivo might be elucidated that ORP could increase expression level of Nrf2 and its downstream ARE gene battery in the testis, promote production of corresponding antioxidative enzymes and protein, and enhance Keap1-Nrf2/ARE signaling pathway to avoid male reproductive dysfunction. In addition, ORP treatment could improve survival capacity of H2O2-induced TM4 cells and its antioxidant mechanism in vitro also had been verified to activate Keap1-Nrf2/ARE signaling pathway. Overall, these results showed that ORP as a potent antioxidant could reduce reproductive oxidative stress damage related to Keap1-Nrf2/ARE pathway.
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