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CLC number: Q25; Q492

On-line Access: 2024-08-27

Received: 2023-10-17

Revision Accepted: 2024-05-08

Crosschecked: 2009-01-04

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Journal of Zhejiang University SCIENCE B 2009 Vol.10 No.2 P.87-92

http://doi.org/10.1631/jzus.B0820133


Ginsenosides stimulated the proliferation of mouse spermatogonia involving activation of protein kinase C


Author(s):  Da-lei ZHANG, Kai-ming WANG, Cai-qiao ZHANG

Affiliation(s):  Key Laboratory of Animal Epidemic Etiology and Immunological Prevention of the Ministry of Agriculture, College of Animal Sciences, Zhejiang University, Hangzhou 310029, China; more

Corresponding email(s):   cqzhang@zju.edu.cn

Key Words:  Ginsenosides, Spermatogonia, Protein kinase C, Mouse


Da-lei ZHANG, Kai-ming WANG, Cai-qiao ZHANG. Ginsenosides stimulated the proliferation of mouse spermatogonia involving activation of protein kinase C[J]. Journal of Zhejiang University Science B, 2009, 10(2): 87-92.

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DOI - 10.1631/jzus.B0820133


Abstract: 
The effect of ginsenosides on proliferation of type A spermatogonia was investigated in 7-day-old mice. spermatogonia were characterized by c-kit expression and cell proliferation was assessed by immunocytochemical demonstration of proliferating cell nuclear antigen (PCNA). After 72-h culture, Sertoli cells formed a confluent monolayer to which numerous spermatogonial colonies attached. spermatogonia were positive for c-kit staining and showed high proliferating activity by PCNA expression. ginsenosides (1.0~10 μg/ml) significantly stimulated proliferation of spermatogonia. Activation of protein kinase C (PKC) elicited proliferation of spermatogonia at 10−8 to 10−7 mol/L and the PKC inhibitor H7 inhibited this effect. Likewise, ginsenosides-stimulated spermatogonial proliferation was suppressed by combined treatment of H7. These results indicate that the proliferating effect of ginsenosides on mouse type A spermatogonia might be mediated by a mechanism involving the PKC signal transduction pathway.

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article

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