Anti-frostbite effect of miglitol on cold-exposed mice through UCP1-mediated thermogenic activation
Objective To investigate the effect and mechanism of miglitol on regulating the energy metabolism of brown adipocytes by activating UCP1 and preventing cold injury in mice after cold exposure.Methods Primary brown adipocytes were induced into mature adipocytes,the effect of miglitol on the viability of brown adipocytes was investigated by MTT method,the lipid droplet consumption level of cells after drug administration was investigated by Oil Red O staining technology,and the level of UCP1,a key protein of thermogenesis in brown adipocytes,was detected by Western blotting.The activity of anti-frostbite was investigated in cold exposure at 4℃and-20℃.KM mice,which were randomly divided into control group,cold exposure group,miglitol group and all-trans retinoic acid group,and after 7 days of repeated administration,the body surface temperature of mice was detected by infrared thermal imaging system,the anal temperature change was detected by anal thermometer,and the expression levels of UCP1 and PGC1-α in adipose tissue were detected by immunoblotting.Results Compared with the control group,the lipid droplet consumption and UCP1 expression levels in brown adipocytes in the miglitol group were significantly increased.The levels of body surface temperature and rectal temperature increased significantly after cold exposure,and the levels of UCP1 and PGC1α in the brown adipose tissue of mice increased significantly,which indicated that the miglitol could activate the critical proteins UCP1 and PGC1α of the thermogenesis pathway,increase the thermogenesis of mice after cold exposure,and thus improve the effect of cold injury for toe swelling.Conclusion Miglitol could play a role in improving cold injury and body temperature in mice by increasing the level of UCP1 and PGC1α,which are key targets of the thermogenesis pathway to promote the thermogenesis of brown fat.
万方数据
维普
