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논문 기본 정보

자료유형
학술저널
저자정보
Kim Min Ju (Jeonju AgroBio-Materials Institute Jeonju 54810 Republic of Korea) Hurh Joon (Chebigen Co. Ltd. Jeonju 54853 Republic of Korea) Kim Ha-Rim (Jeonju AgroBio-Materials Institute Jeonju 54810 Republic of Korea) Lee Sang-Wang (Chebigen Co. Ltd. Jeonju 54853 Republic of Korea) Sin Hong-Sig (Chebigen Co. Ltd. Jeonju 54853 Republic of Korea) Kim Sang-Jun (Jeonju AgroBio-Materials Institute Jeonju 54810 Republic of Korea) Noh Eun-mi (Jeonju AgroBio-Materials Institute Jeonju 54810 Republic of Korea) Oh Boung-Jun (Jeonju AgroBio-Materials Institute Jeonju 54810 Republic of Korea) Kim Seon-Young (Jeonju AgroBio-Materials Institute Jeonju 54810 Republic of Korea)
저널정보
한국미생물생명공학회 Journal of Microbiology and Biotechnology Journal of Microbiology and Biotechnology 제33권 제4호
발행연도
2023.4
수록면
463 - 470 (8page)
DOI
10.4014/jmb.2211.11044

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This study confirmed the change in functional composition and alcohol-induced acute liver injury in Aloe arborescens after fermentation. An acute liver injury was induced by administration of ethanol (3 g/kg/day) to C57BL/6J mice for 5 days. A fermented A. arborescens Miller leaf (FAAL) extract was orally administered 30 minutes before ethanol treatment. After fermentation, the emodin content was approximately 13 times higher than that of the raw material. FAAL extract significantly attenuated ethanol-induced aspartate aminotransferase, alanine aminotransferase, and triglyceride increases in serum and liver tissue. Histological analysis revealed that FAAL extract inhibits inflammatory cell infiltration and fat accumulation in liver tissues. The cytochrome P450 2E1, superoxide dismutase, and glutathione (GSH), which involved in alcohol-induced oxidative stress, were effectively regulated by FAAL extract in serum and liver tissues, except for GSH. FAAL also maintained the antioxidant defense system by upregulating heme oxygenase 1 and nuclear factor erythroid 2-related factor 2 protein expression. In addition, FAAL extract inhibited the decrease in alcohol dehydrogenase and aldehyde dehydrogenase activity, which promoted alcohol metabolism and prevented the activation of inflammatory response. Our results suggest that FAAL could be used as a potential therapeutic agent for ethanol-induced acute liver injury.

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