Beneficial effects of fermented black ginseng and its ginsenoside 20(S)-Rg3 against cisplatin-induced nephrotoxicity in LLC-PK1 cells

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• 作者：Myoung-Sik Han¹ ; ^☆ ; Im-Ho Han² ; ³ ; ^☆ ; Dahae Lee⁴ ; Jun Min An⁵ ; Su-Nam Kim³ ; Myoung-Sook Shin³ ; Noriko Yamabe⁴ ; Gwi Seo Hwang⁴ ; Hye Hyun Yoo⁶ ; Suk-Jung Choi² ; Ki Sung Kang⁴ ; ^{kkang@gachon.ac.kr" class="auth_mail" title="E-mail the corresponding author} ; Hyuk-Jai Jang¹ ; ^{jhj@gnah.co.kr" class="auth_mail" title="E-mail the corresponding author}
• 关键词：cisplatin ; ginsenoside 20(S)-Rg3 ; mitogen-activated protein kinases ; nephrotoxicity ; Panax ginseng
• 刊名：Journal of Ginseng Research
• 出版年：2016
• 出版时间：April 2016
• 年：2016
• 卷：40
• 期：2
• 页码：135-140
• 全文大小：1024 K

文摘

Nephrotoxicity is a common side effect of medications. Panax ginseng is one of the best-known herbal medicines, and its individual constituents enhance renal function. Identification of its efficacy and mechanisms of action against drug-induced nephrotoxicity, as well as the specific constituents mediating this effect, have recently emerged as an interesting research area focusing on the kidney protective efficacy of P. ginseng.

Methods

The present study investigated the kidney protective effect of fermented black ginseng (FBG) and its active component ginsenoside 20(S)-Rg3 against cisplatin (chemotherapy drug)-induced damage in pig kidney (LLC-PK1) cells. It focused on assessing the role of mitogen-activated protein kinases as important mechanistic elements in kidney protection.

Results

The reduced cell viability induced by cisplatin was significantly recovered with FBG extract and ginsenoside 20(S)-Rg3 dose-dependently. The cisplatin-induced elevated protein levels of phosphorylated c-Jun N-terminal kinase (JNK), p53, and cleaved caspase-3 were decreased after cotreatment with FBG extract or ginsenoside 20(S)-Rg3. The elevated percentage of apoptotic LLC-PK1 cells induced by cisplatin treatment was significantly abrogated by cotreatment with FBG and the ginsenoside 20(S)-Rg3.

Conclusion

FBG and its major ginsenoside 20(S)-Rg3, ameliorated cisplatin-induced nephrotoxicity in LLC-PK1 cells by blocking the JNK–p53–caspase-3 signaling cascade.