Short communication. Enhancement of the immune responses to vaccination against foot-and-mouth disease in mice by oral administration of Quillaja saponaria-A and extracts of Cochinchina momordica seed

This study was designed to evaluate the effects of oral administration of extracts from Cochinchina momordica seed (ECMS) or Quillaja saponaria-A (Quil-A) on the immune responses in mice immunized with foot and mouth disease virus (FMDV)-serotype O vaccine. Forty-two imprinting control region (ICR) mice were randomly divided into seven groups of 6 animals in each group, and a dose of 400 ìg of Quil-A or ECMS was orally administered for 1, 2 or 3 days. After that, the animals were subcutaneously immunized twice with FMD vaccine at 3-week intervals and blood samples were collected 2-weeks after boosting for measurement of FMDV-specific IgG and its subclasses. Spleens were collected for lymphocytes proliferation assay. Results indicated that serum FMDV-specific IgG and the IgG subclass responses were significantly enhanced in mice orally administered ECMS or Quil-A when compared with the control group (p < 0.05). Lymphocytes proliferation response to FMD vaccine was significantly enhanced by ECMS compared with the control (p < 0.05). This study illustrates that ECMS induced immunomodulatory effects and performed better than Quil-A

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

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