Betulinic Acid Attenuates T-2-Toxin-Induced Testis Oxidative Damage Through Regulation of the JAK2/STAT3 Signaling Pathway in Mice
by
Jing Wu 1, Chenglin Yang 1, Juan Liu 1, Jiaxin Chen 1, Chao Huang 1, Ji Wang 1, Zengenni Liang 2, Lixin Wen 1, Jin-e Yi 1,* and Zhihang Yuan 1,*
Jing Wu 1, Chenglin Yang 1, Juan Liu 1, Jiaxin Chen 1, Chao Huang 1, Ji Wang 1, Zengenni Liang 2, Lixin Wen 1, Jin-e Yi 1,* and Zhihang Yuan 1,*
1
College of Veterinary Medicine, Hunan Agricultural University, Changsha 410128, China
2
Department of Hunan Agricultural Product Processing Institute, Changsha 410128, China
*
Authors to whom correspondence should be addressed.
Biomolecules 2019, 9(12), 787; https://doi.org/10.3390/biom9120787
Received: 14 October 2019 / Revised: 20 November 2019 / Accepted: 23 November 2019 / Published: 26 November 2019
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.
Keywords:
T-2 toxin; betulinic acid; testis; oxidative stress; apoptosis; JAK2/STAT3 signaling pathway
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited
MDPI and ACS Style
Wu, J.; Yang, C.; Liu, J.; Chen, J.; Huang, C.; Wang, J.; Liang, Z.; Wen, L.; Yi, J.-E.; Yuan, Z. Betulinic Acid Attenuates T-2-Toxin-Induced Testis Oxidative Damage Through Regulation of the JAK2/STAT3 Signaling Pathway in Mice. Biomolecules 2019, 9, 787.
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