The Effects Of Macrophage Migration Inhibitory Factor On Metabolism Of Free-Fatty-Acid In Broiler Chicken Cardiocytes In Hypoxia

[Purpose]The broiler ascites syndromes(AS)reduces the meat quality and economic benefits of the poultry industry.The previous studies focused on hypoxia-induced pulmonary hypertension,however,the pathogenesis was not entirely clear.This disease was a metabolic problem,and right ventricular hypertrophy was the obvious feature.Olkowski group and ours separately found that broiler heart played a important role in AS occurrence,myocardial metabolic remodeling probably initiated the heart failure,and finally sparked ascites.In addition,our previous work has shown that the expression of macrophage migration inhibition factor(MIF)in broiler lungs with pulmonary hypertension was significantly higher than those in healthy broilers,which means that MIF has involved in the development of AS in broilers.The aim of this study was to investigate the effects of MIF on metabolism of Free-Fatty-Acid in broiler chicken cardiocytes in hypoxia.[Methods]Firstly,chicken embryonic cardiomyocytes were isolated by trypsin and type II collagenase,and cultured in DMEM,then identified by a-actinin immunocytochemistry.Secondly,Cobalt chloride induced hypoxia model of chicken cardiocyte was established,which was identified by the hypoxia sign protein--HIF-1?.Thirdly,the MIF blocker ISO-1 was used to test the relationship between MIF and p-AMPK.Finally,in order to confirm whether MIF was involved in myocardial fatty acid metabolism regulation during hypoxia by activating the AMPK,the expression levels of FAT/CD36,p-ACC and CPT-1A in cardiomyocytes were determined by western blot during hypoxia and normoxia.[Results]The chicken cardiocytes,above 90%purity,showed spherical and polygon shape in vivo,and they beat spontaneously about 80-130 times per minute.HIF-la expression reached the highest at 24 h with the 600 ?M CoCl2.The levels of MIF,p-AMPK,FAT/CD36,p-ACC and CPT-1A were all increased significantly(P<0.01)in the hypoxia group compared with the normal one,and the p-AMPK,FAT/CD36,p-ACC and CPT-1A levels decreased significantly(P<0.01)along with the MIF which was blocked by 100 ?M ISO-1,[Conclusion]MIF,a myocardial autocrine factor,plays an important protective role in the fatty acid adapted metabolism of chicken cardiomyocytes during hypoxia by activating the AMPK signal pathway.