Betulinic Acid Attenuates T-2-Toxin-Induced Testis Oxidative Damage Through Regulation of the JAK2/STAT3 Signaling Pathway in Mice
文献类型： 外文期刊
作者： Wu, Jing 1 ; Yang, Chenglin 1 ; Liu, Juan 1 ; Chen, Jiaxin 1 ; Huang, Chao 1 ; Wang, Ji 1 ; Liang, Zengenni 2 ; Wen, Lixi 1 ;
作者机构： 1.Hunan Agr Univ, Coll Vet Med, Changsha 410128, Peoples R China
2.Dept Hunan Agr Prod Proc Inst, Changsha 410128, Peoples R China
关键词： T-2 toxin; betulinic acid; testis; oxidative stress; apoptosis; JAK2; STAT3 signaling pathway
期刊名称：BIOMOLECULES （ 影响因子：4.879； 五年影响因子：5.362 ）
ISSN：
年卷期： 2019 年 9 卷 12 期
页码：
收录情况： SCI
摘要： T-2 toxin is one of the most toxic type A trichothecene mycotoxins in nature, and it exhibits reproductive toxicity. Betulinic acid (BA) is a natural pentacyclic triterpene compound found in species of Betula, and it has been reported to have antioxidant activity. The aim of the present study was to investigate the protective effect of BA on T-2-toxin-induced testicular injury in mice and explore its molecular mechanism. Sixty adult male mice were randomly divided into groups. The mice were pretreated orally with BA (0.25, 0.5, and 1.0 mg/kg) daily for 14 days, and the T-2 toxin (4 mg/kg body weight) was administered via intraperitoneal injection to induce oxidative stress after the last administration of BA. BA pretreatment significantly increased the secreted levels of testosterone and sperm motility. Moreover, BA pretreatment significantly increased the total antioxidant capacity (T-AOC), the activity of SOD and CAT, and the content of GSH, and it reduced the content of MDA. Furthermore, BA relieved testicular injury and reduced the number of apoptotic cells, and it significantly decreased the protein expression of Janus kinase 2 (JAK2), signal transducers and activators of transcription 3 (STAT3), caspsae-3, and Bcl-2-associated X protein (Bax). BA also increased the expression of B-cell lymphoma-2 (Bcl-2). We suggest that BA reduced the oxidative damage induced by T-2 toxin, and that these protective effects may be partially mediated by the JAK2/STAT3 signaling pathway.
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