2. Academic Validation
  3. Hederagenin Supplementation Alleviates the Pro-Inflammatory and Apoptotic Response to Alcohol in Rats

Hederagenin Supplementation Alleviates the Pro-Inflammatory and Apoptotic Response to Alcohol in Rats

  • Nutrients. 2017 Jan 6;9(1):41. doi: 10.3390/nu9010041.
Gyeong-Ji Kim 1,  Da Hye Song 2,  Han Seok Yoo 3,  Kang-Hyun Chung 4,  Kwon Jai Lee 5,  Jeung Hee An 6
Affiliations

Affiliations

  • 1 Division of Food Bioscience, Konkuk University, Chunju 27478, Korea. kgj8495@hanmail.net.
  • 2 Division of Food Bioscience, Konkuk University, Chunju 27478, Korea. sdh5740@naver.com.
  • 3 Department of Food Science and Technology, Seoul National University of Science & Technology, Seoul 01811, Korea. yhs0223@naver.com.
  • 4 Department of Food Science and Technology, Seoul National University of Science & Technology, Seoul 01811, Korea. carl@seoultech.ac.kr.
  • 5 Department of Advanced Materials Engineering, Daejeon University, Daejeon 34520, Korea. jmul@ssu.ac.kr.
  • 6 Division of Food Bioscience, Konkuk University, Chunju 27478, Korea. anjhee@hanmail.net.
PMID: 28067819 DOI: 10.3390/nu9010041
Abstract

In this study, we determined the effects of hederagenin isolated from Akebia quinata fruit on alcohol-induced hepatotoxicity in rats. Specifically, we investigated the hepatoprotective, anti-inflammatory, and anti-apoptotic effects of hederagenin, as well as the role of Akt and mitogen-activated protein kinase (MAPK) signaling pathways in ethanol-induced liver injury. Experimental Animals were randomly divided into three groups: normal (sham), 25% ethanol, and 25% ethanol + hederagenin (50 mg/kg/day). Each group was orally administered the respective treatments once per day for 21 days. Acetaldehyde dehydrogenase-2 mRNA expression was higher and alcohol dehydrogenase mRNA expression was lower in the ethanol + hederagenin group than those in the ethanol group. Pro-inflammatory cytokines, including TNF-α, IL-6, and cyclooxygenase-2, significantly increased in the ethanol group, but these increases were attenuated by hederagenin. Moreover, Western blot analysis showed increased expression of the apoptosis-associated protein, Bcl-2, and decreased expression of Bax and p53 after treatment with hederagenin. Hederagenin treatment attenuated ethanol-induced increases in activated p38 MAPK and increased the levels of phosphorylated Akt and ERK. Hederagenin alleviated ethanol-induced liver damage through anti-inflammatory and anti-apoptotic activities. These results suggest that hederagenin is a potential candidate for preventing alcoholic liver injury.

Keywords

ALDH2; alcohol; apoptosis; hederagenin; inflammatory; liver disease.

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