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Increased hepatic mitophagy by acute alcohol feeding ameliorates liver injury in rats: involvement of thehypoxia-inducible factor-1á pathway

Author(s): M.A.Guodong, Su Wen, Wang Manzhuo, Liu Yanhuan

Mitophagy plays key roles in the process of acute alcoholic liver injury. Many studies show that HIF-1á may exert direct or indirect effects on liver injury. However, whether HIF-1á can interfere with liver mitophagy remains elusive. The rats were randomly divided into four groups: (1) control group(C); (2) 3-(5′-hydroxymethyl-2′-furyl)-1- benzylindazole (YC-1) group (CY); (3) five-day alcohol intake group (CA); and (4) fiveday- alcohol intake plus YC-1 group (CAY). The rats were investigated to determine the following: BNIP3, HIF-1á, LC3II, Beclin1 mRNA and protein expressions; mitochondrial ROS production; mitochondrial TBARS level; aconitase and ATP synthase activities; mitochondrial inner membrane potential; the number of mtDNA and mitochondrial respiration functions in liver tissue; and serum ALT and AST. The results showed that acute alcohol intake caused significant increased HIF1-á, BNIP3, LC3II and Beclin1 levels and decreased mtDNA copy number. Meanwhile, mitochondrial oxidative injury increased with decreased respiratory function. Added HIF1-á inhibitor resulted in significantly lower HIF1-á, BNIP3, LC3II and Beclin1 expression and increased mtDNA copy number compared to the single acute alcohol intake. However, mitochondrial oxidative injury further increased with further decreased respiratory function. It showed that acute alcohol consumption induced mitophagy may involve the HIF-1a pathway, which can ameliorate liver injury. However, it was not enough to completely clear the damaged mitochondria, resulting in acute alcoholic liver injury in rats.

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