Biotechnology |
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Ginsenosides stimulated the proliferation of mouse spermatogonia involving activation of protein kinase C |
Da-lei ZHANG, Kai-ming WANG, Cai-qiao ZHANG |
Key Laboratory of Animal Epidemic Etiology and Immunological Prevention of the Ministry of Agriculture, College of Animal Sciences, Zhejiang University, Hangzhou 310029, China; College of Medicine, Nanchang University, Nanchang 330006, China |
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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.
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Received: 24 April 2008
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