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Toxins (Basel). 2018 Jun 9;10(6). pii: E235. doi: 10.3390/toxins10060235.

Resveratrol Ameliorates Microcystin-LR-Induced Testis Germ Cell Apoptosis in Rats via SIRT1 Signaling Pathway Activation.

Author information

1
College of Public Health, Zhengzhou University, Zhengzhou 450001, China. Liuhlin2018@126.com.
2
College of Public Health, Zhengzhou University, Zhengzhou 450001, China. zsslb2005@163.com.
3
College of Public Health, Zhengzhou University, Zhengzhou 450001, China. lcr0624@126.com.
4
College of Public Health, Zhengzhou University, Zhengzhou 450001, China. wjxsir@126.com.
5
College of Public Health, Zhengzhou University, Zhengzhou 450001, China. wyq2018@stu.zzu.edu.cn.
6
College of Public Health, Zhengzhou University, Zhengzhou 450001, China. yl19920215@126.com.
7
College of Public Health, Zhengzhou University, Zhengzhou 450001, China. dxd1993@163.com.
8
College of Public Health, Zhengzhou University, Zhengzhou 450001, China. wr935314032@163.com.
9
College of Public Health, Zhengzhou University, Zhengzhou 450001, China. wegesalee@gmail.com.
10
College of Public Health, Zhengzhou University, Zhengzhou 450001, China. zdg@zzu.edu.cn.
11
College of Public Health, Zhengzhou University, Zhengzhou 450001, China. cxm@zzu.edu.cn.
12
College of Public Health, Zhengzhou University, Zhengzhou 450001, China. huizhenzhang@zzu.edu.cn.

Abstract

Microcystin-leucine arginine (MC-LR), a cyclic heptapeptide produced by cyanobacteria, is a strong reproductive toxin. Studies performed in rat Sertoli cells and Chinese hamster ovary cells have demonstrated typical apoptosis after MC-LR exposure. However, little is known on how to protect against the reproductive toxicity induced by MC-LR. The present study aimed to explore the possible molecular mechanism underlying the anti-apoptosis and protective effects of resveratrol (RES) on the co-culture of Sertoli⁻germ cells and rat testes. The results demonstrated that MC-LR treatment inhibited the proliferation of Sertoli⁻germ cells and induced apoptosis. Furthermore, sirtuin 1 (SIRT1) and Bcl-2 were inhibited, while p53 and Ku70 acetylation, Bax expression, and cleaved caspase-3 were upregulated by MC-LR. However, RES pretreatment ameliorated MC-LR-induced apoptosis and SIRT1 inhibition, and downregulated the MC-LR-induced increase in p53 and Ku70 acetylation, Bax expression, and caspase-3 activation. In addition, RES reversed the MC-LR-mediated reduction in Ku70 binding to Bax. The present study indicated that the administration of RES could ameliorate MC-LR-induced Sertoli⁻germ cell apoptosis and protect against reproductive toxicity in rats by stimulating the SIRT1/p53 pathway, suppressing p53 and Ku70 acetylation and enhancing the binding of Ku70 to Bax.

KEYWORDS:

apoptosis; microcystin-LR (MC-LR); reproductive toxicity; resveratrol; sirtuin 1 (SIRT1)

PMID:
29890735
PMCID:
PMC6024601
DOI:
10.3390/toxins10060235
[Indexed for MEDLINE]
Free PMC Article

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