Protective effect of resveratrol derivatives on high-fat diet induced fatty liver by activating AMP-activated protein kinase

Choi, You-Jin; Suh, Hyo-Ryung; Yoon, Yujin; Lee, Kyung-Jin; Kim, Dong Gwang; Kim, Sanghee; Lee, Byung-Hoon

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자료유형: 학술저널

저자정보: Choi, You-Jin (College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University) Suh, Hyo-Ryung (College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University) Yoon, Yujin (College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University) Lee, Kyung-Jin (College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University) Kim, Dong Gwang (College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University) Kim, Sanghee (College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University) Lee, Byung-Hoon (College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University)

저널정보: 대한약학회 Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea 제37권 제9호

발행연도: 2014.1

수록면: 1,169 - 1,176 (8page)

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Non-alcoholic fatty liver disease is associated with inhibited AMP-activated kinase (AMPK) and activation of sterol regulatory element binding protein 1 (SREBP-1). AMPK phosphorylation inhibits SREBP-1, a major transcription factor of de novo lipogenesis, by inhibiting the liver X receptor (LXR) or by direct phosphorylation. Resveratrol, a polyphenol, has regulatory effects on hepatic lipid metabolism as a potent AMPK activator. In this study, we evaluated the anti-steatogenic effects of resveratrol and its derivatives and identified the molecular mechanism in vitro and in vivo. Resveratrol and its derivatives decreased lipid accumulation by free fatty acids (FFA mixture; 0.5 mM, oleic acid:palmitic acid = 2:1) in H4IIEC3 cells. Synthesized derivatives of resveratrol had lower cytotoxicity than the parental molecule with similar potency. SY-102 suppressed SREBP-1 maturation by T0901317, an LXR agonist, and decreased SRE luciferase activity and the mRNA levels of lipogenic genes. Inhibition of AMPK by pre-treatment with compound C completely blocked the effects of SY-102. To evaluate their efficacy in vivo, mice were fed a high-fat diet for 5 days, and resveratrol or SY-102 was administered orally for the last 2 days. Oral administration of the SY-102 increased AMPK phosphorylation, followed by reduced hepatic triglyceride accumulation to a similar extent as resveratrol. These data demonstrate that SY-102, a synthesized derivative of resveratrol, might provide a promising therapeutic effect against fatty liver disease.

#Resveratrol derivatives #NAFLD #AMPK #High-fat diet

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