文摘

增加了急性酒精肝mitophagy喂养改善大鼠肝损伤:参与thehypoxia-inducible factor-1Aƒ¡通路

作者(年代):硕士国栋,苏温家宝,王Manzhuo,刘Yanhuan

Mitophagy扮演关键角色的过程中急性酒精性肝损伤。许多研究表明,HIF-1a可能施加直接或间接对肝损伤的影响。然而,HIF-1a能否干扰肝脏mitophagy仍然遥遥无期。老鼠被随机分为4组:对照组(1)(C);(2)3 - (5′-hydroxymethyl-2′-furyl) 1 - benzylindazole (YC-1)组(CY);(3)五天饮酒组(CA);(4)fiveday -饮酒+ YC-1集团(礁)。老鼠研究决定如下:BNIP3, HIF-1a, LC3II, Beclin1 mRNA和蛋白表达;线粒体ROS生产;线粒体TBARS水平; 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.