Anticancer effect of joboksansam, Korean wild ginseng germinated from bird feces

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• 作者：Jae Gwang Park¹ ; ^☆ ; Wie-Soo Kang² ; ^☆ ; Kyung Tae Park³ ; Dong Jun Park³ ; Adithan Aravinthan⁴ ; Jong-Hoon Kim⁴ ; ^{jhkim1@chonbuk.ac.kr" class="auth_mail" title="E-mail the corresponding author} ; Jae Youl Cho¹ ; ^{jaecho@skku.edu" class="auth_mail" title="E-mail the corresponding author}
• 关键词：anticancer activity ; cytotoxicity ; joboksansam ; Panax ginseng ; survival enzyme
• 刊名：Journal of Ginseng Research
• 出版年：2016
• 出版时间：July 2016
• 年：2016
• 卷：40
• 期：3
• 页码：304-308
• 全文大小：546 K

文摘

Joboksansam, Korean bird wild ginseng, is an artificially cultivated wild ginseng germinated from bird feces. Although numerous pharmacologic activities of wild ginsengs have been reported, the beneficial effect of joboksansam in cancer has not been elucidated. In this study, we investigated the in vivo and in vitro anticancer activities of joboksansam powder.

Methods

To evaluate the in vivo anticancer activity of joboksansam, we established a xenograft mouse model bearing RMA cell-derived cancer. Direct cytotoxicity induced by joboksansam powder was also investigated in vitro using (3-4-5-dimethylthiazol-2-yl)-2-5-diphenyltetrazolium bromide (MTT) assay. The inhibitory activity of this powder on the activation of cell survival signaling involving Akt and Src was examined with immunoblot analysis.

Results

Joboksansam powder displayed strong inhibitory activity against the increased tumor size, increased weight of total body and cancer tissues, and mortality of tumor-bearing mice. Joboksansam powder also suppressed the activation of survival regulatory enzymes Akt and Src, as assessed by phosphorylation levels in the immunoblot analysis of tumor tissues. Interestingly, the viability of RMA cells in vitro was directly decreased by joboksansam treatment.

Conclusion

Overall, our results strongly suggest that joboksansam powder has the potential to protect against cancer generation by direct cytotoxic effects on cancer cells resulting from suppression of cell survival signaling.