Open Access

ARTICLE

Inhibition of H₂O₂-induced TM3 cell apoptosis by oxidative stress by lentinan functionalized selenium nanoparticles through JAK2/STAT-3 and P53 pathways

MIAOMIAO LI^1,#, ZILIN ZHENG^1,#, JUNYI KE¹, JIEYI LUO¹, FAN JIANG¹, YANXIA QU¹, BING ZHU², YINGHUA LI^2,*, LIANDONG ZUO^1,*

1 Department of Andrology, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangzhou, 510120, China
2 Center Laboratory, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangzhou, 510120, China

* Corresponding Authors: YINGHUA LI. Email: ; LIANDONG ZUO. Email:
# Miaomiao Li and Zilin Zheng contributed equally to the work

BIOCELL 2023, 47(6), 1397-1405. https://doi.org/10.32604/biocell.2023.027971

Received 24 November 2022; Accepted 10 February 2023; Issue published 19 May 2023

Abstract

Background: Nano-selenium has been widely used in antiviral and anticancer therapy, and has the advantages of good targeting and low toxicity. For the first time, we combined male reproduction with nano-selenium to investigate its antioxidant effect. This study investigated the protective effect of lentinan functionalized selenium nanoparticles on oxidative stress injury of the hydrogen peroxide (H₂O₂)-induced Leydig cell line, TM3. Methods: The suitable concentration of nano-selenium treatment to promote cell proliferation was also discussed. The concentration of 4 μM could significantly promote the growth of TM3 cells. Oxidative stress damage was caused using an 800 μM concentration of hydrogen peroxide. The cells were divided into four groups: normal control group, oxidative stress treatment group, H₂O₂+SeNPs@LNT group, and SeNPs@LNT group. The H₂O₂+SeNPs@LNT group was pretreated with 4 μM of SeNPs@LNT for 12 h, followed by 800 μM of H₂O₂ for 8 h. Results: Nano-selenium could significantly promote the proliferation and viability of TM3 cells. SeNPs@LNT treatment increased the level of mitochondrial membrane potential in normal cells and slowed down the decline in mitochondrial membrane potential level caused by oxidative stress injury. In addition, the increase in reactive oxygen species caused by oxidative stress was inhibited by SeNPs@LNT treatment. The apoptosis of TM3 cells was detected, and SeNPs@LNT alleviated the necrosis and apoptosis of TM3 cells induced by H₂O₂. Nano-selenium plays a protective role against oxidative H₂O₂-induced stress injury in TM3 cells through the changes in the Janus kinase 2/signal transducer and activator of transcription 3 signaling pathway and P53 pathway, and the expression levels of other related proteins, protein kinase B (AKT) and C3. Conclusion: SeNPs@LNT exhibited good biological activity and antioxidant effect and can thus be used to protect the male reproductive system from oxidative stress.

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