Journal
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
Volume 68, Issue 44, Pages 12284-12294Publisher
AMER CHEMICAL SOC
DOI: 10.1021/acs.jafc.0c04539
Keywords
alcoholic liver disease; rice bran phenolic extract; mitochondrial dysfunction; PGC-1 alpha; TFAM; microRNA-494
Funding
- Key Research and Development Program of Guangdong Province [2020B020225004]
- National Natural Science Foundation of China [31960483, 31972082]
- Scientific Research Startup fund of Hainan University [KYQD(ZR) 1804]
- Guangdong Special Support Program [2019BT02N112]
- Group Program of Natural Science Foundation of Guangdong Province [2016A030312001]
- Special Fund for Scientific Innovation Strategy-Construction of High level Academy of Agriculture Science [R2018PY-JC002]
- Discipline Team Building Projects of Guangdong Academy of Agricultural Sciences in the 13th Five-Year Period [201602TD]
- Open Fund of Key Laboratory of Food Nutrition and Functional Food of Hainan Province [KF202009]
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The initiation and development of alcoholic liver disease (ALD) is mediated, at least partly, by mitochondria dysfunction, which is regulated by PPAR gamma coactivator-1a (PGC-1 alpha) via mitochondria transcription factor A (TFAM). Then, PGC-1 alpha expression was regulated by several microRNAs. This research investigated the hepatoprotective effects of the rice bran phenolic extract (RBPE) on mice fed with an ethanol-containing diet via the microRNAs-PGC-1a-TFAM signal pathway. RBPE treatment protected against alcoholic liver injury, as indicated by decreased serum aminotransferase activities and hepatic triglyceride accumulation, together with alleviated oxidative stress in serum and the liver. RBPE treatment alleviated ethanol-induced mitochondrial dysfunction through altering the membrane potential, mtDNA content, and respiratory chain complex enzyme activities in mitochondria, resulting in increased hepatic ATP production. Decreased cytoplasmic cytochrome c contents, caspase-3 activity, and Bax/BcI-2 ratio were detected in the liver of RBPE-treated mice, indicating that the RBPE might inhibit ethanol-induced hepatocellular apoptosis. Furthermore, ethanol-induced decreases in the mRNA and protein expression of PGC-la and TFAM were remarkably alleviated in RBPE-treated mice. RBPE treatment to ethanol-fed mice could also downregulate the expression of microRNA-494-3p, which regulates PGC-1 alpha expression directly. Therefore, the RBPE might exert protection against ALD by alleviating mitochondrial dysfunction and the resulting hepatocyte apoptosis via the PGC-1 alpha-TFAM signal pathway mediated by microRNA-494-3p.
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