DOI QR코드

DOI QR Code

Fermented Protaetia brevitarsis Larvae Ameliorates Chronic Ethanol-Induced Hepatotoxicity in Mice via AMPK and TLR-4/TGF-β1 Pathways

  • Hyo Lim Lee (Division of Applied Life Science (BK21), Institute of Agriculture and Life Science, Gyeongsang National University) ;
  • Jong Min Kim (Division of Applied Life Science (BK21), Institute of Agriculture and Life Science, Gyeongsang National University) ;
  • Min Ji Go (Division of Applied Life Science (BK21), Institute of Agriculture and Life Science, Gyeongsang National University) ;
  • Seung Gyum Joo (Division of Applied Life Science (BK21), Institute of Agriculture and Life Science, Gyeongsang National University) ;
  • Tae Yoon Kim (Division of Applied Life Science (BK21), Institute of Agriculture and Life Science, Gyeongsang National University) ;
  • Han Su Lee (Division of Applied Life Science (BK21), Institute of Agriculture and Life Science, Gyeongsang National University) ;
  • Ju Hui Kim (Division of Applied Life Science (BK21), Institute of Agriculture and Life Science, Gyeongsang National University) ;
  • Jin-Sung Son (HMO Health Dream Agricultural Association Corporation) ;
  • Ho Jin Heo (Division of Applied Life Science (BK21), Institute of Agriculture and Life Science, Gyeongsang National University)
  • 투고 : 2023.10.04
  • 심사 : 2023.10.30
  • 발행 : 2024.03.28

초록

This study evaluated the hepatoprotective effect of fermented Protaetia brevitarsis larvae (FPB) in ethanol-induced liver injury mice. As a result of amino acids in FPB, 18 types of amino acids including essential amino acids were identified. In the results of in vitro tests, FPB increased alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) activities. In addition, FPB treatment increased cell viability on ethanol- and H2O2-induced HepG2 cells. FPB ameliorated serum biomarkers related to hepatoxicity including glutamic oxaloacetic transaminase, glutamine pyruvic transaminase, total bilirubin, and lactate dehydrogenase and lipid metabolism including triglyceride, total cholesterol, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol. Also, FPB controlled ethanol metabolism enzymes by regulating the protein expression levels of ADH, ALDH, and cytochrome P450 2E1 in liver tissue. FPB protected hepatic oxidative stress by improving malondialdehyde content, reduced glutathione, and superoxide dismutase levels. In addition, FPB reversed mitochondrial dysfunction by regulating reactive oxygen species production, mitochondrial membrane potential, and ATP levels. FPB protected ethanol-induced apoptosis, fatty liver, and hepatic inflammation through p-AMP-activated protein kinase and TLR-4/NF-κB signaling pathways. Furthermore, FPB prevented hepatic fibrosis by decreasing TGF-β1/Smad pathway. In summary, these results suggest that FPB might be a potential prophylactic agent for the treatment of alcoholic liver disease via preventing liver injury such as fatty liver, hepatic inflammation due to chronic ethanol-induced oxidative stress.

키워드

과제정보

This study was supported by the Technology development Program (S3269035) funded by the Ministry of SMEs and Startups (MSS), Korea.

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