Open Access iconOpen Access

ARTICLE

crossmark

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

MIAOMIAO LI1,#, ZILIN ZHENG1,#, JUNYI KE1, JIEYI LUO1, FAN JIANG1, YANXIA QU1, BING ZHU2, YINGHUA LI2,*, LIANDONG ZUO1,*

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: email; LIANDONG ZUO. Email: 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

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.

Keywords


Cite This Article

APA Style
LI, M., ZHENG, Z., KE, J., LUO, J., JIANG, F. et al. (2023). Inhibition of h2o2-induced TM3 cell apoptosis by oxidative stress by lentinan functionalized selenium nanoparticles through JAK2/STAT-3 and P53 pathways. BIOCELL, 47(6), 1397-1405. https://doi.org/10.32604/biocell.2023.027971
Vancouver Style
LI M, ZHENG Z, KE J, LUO J, JIANG F, QU Y, et al. Inhibition of h2o2-induced TM3 cell apoptosis by oxidative stress by lentinan functionalized selenium nanoparticles through JAK2/STAT-3 and P53 pathways. BIOCELL . 2023;47(6):1397-1405 https://doi.org/10.32604/biocell.2023.027971
IEEE Style
M. LI et al., “Inhibition of H2O2-induced TM3 cell apoptosis by oxidative stress by lentinan functionalized selenium nanoparticles through JAK2/STAT-3 and P53 pathways,” BIOCELL , vol. 47, no. 6, pp. 1397-1405, 2023. https://doi.org/10.32604/biocell.2023.027971



cc Copyright © 2023 The Author(s). Published by Tech Science Press.
This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
  • 897

    View

  • 500

    Download

  • 0

    Like

Share Link