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Ginsenoside Rg3 protects mouse leydig cells against triptolide by downregulation of miR-26a

Authors Liang H, Zhang S, Li Z

Received 11 March 2019

Accepted for publication 20 May 2019

Published 24 June 2019 Volume 2019:13 Pages 2057—2066

DOI https://doi.org/10.2147/DDDT.S208328

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Palas Chanda

Peer reviewer comments 2

Editor who approved publication: Dr Anastasios Lymperopoulos


Haiyan Liang,1 Suwei Zhang,2 Zhiling Li1

1Reproductive Center, The First Affiliated Hospital of Shantou University Medical College, Shantou University, Shantou, Guangdong 515031, People’s Republic of China; 2Department of Clinical Laboratory Medicine, Shantou Central Hospital, Shantou, Guangdong 515031, People’s Republic of China

Background: Ginsenoside Rg3 has been reported to exert protection function on germ cells. However, the mechanisms by which Rg3 regulates apoptosis in mouse Leydig cells remain unclear. In addition, triptolide (TP) has been reported to induce infertility in male rats. Thus, this study aimed to investigate the protective effect of Rg3 against TP-induced toxicity in MLTC-1 cells.
Methods: CCK-8, immunofluorescence assay, Western blotting and flow cytometry were used to detect cell proliferation and cell apoptosis, respectively. In addition, the dual luciferase reporter system assay was used to detect the interaction between miR-26a and GSK3β in MLTC-1 cells.
Results: TP significantly inhibited the proliferation of MLTC-1 cells, while the inhibitory effect of TP was reversed by Rg3. In addition, TP markedly induced apoptosis in MLTC-1 cells via increasing the expressions of Bax, active caspase 3, Cyto c and active caspase 9, and decreasing the level of Bcl-2. However, Rg3 alleviated TP-induced apoptosis of MLTC-1 cells. Moreover, the level of miR-26a was obviously downregulated by Rg3 treatment. The protective effect of Rg3 against TP-induced toxicity in MLTC-1 cells was abolished by miR-26a upregulation. Meanwhile, dual-luciferase assay showed GSK3β was the direct target of miR-26a in MLTC-1 cells. Overexpression of miR-26a markedly decreased the level of GSK3β. As expected, upregulation of miR-26a could abrogate the protective effects of Rg3 against TP-induced cytotoxicity via inhibiting the expression of GSK3β.
Conclusion: These results indicated that Rg3 could protect MLTC-1 against TP by downregulation of miR-26a. Therefore, Rg3 might serve as a potential agent for the treatment of male hypogonadism.

Keywords: ginsenoside Rg3, male hypogonadism, triptolide, MLTC-1 cell, apoptosis


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