الملخص
Objective To investigate the function of sodium hydrosulfide(NaHS)to regulate mitochondrial fusion/fission in diabetic cardiomyopathy and underlying mechanism.Methods Db/db mice as type 2 diabetes animal model were treated by NaHS.H9C2 cells incubated with glucose(40 mmol/L),palmitic acid(200 μmol/L,Pal)and oleate(200 μmol/L,Ole)were intervened by NaHS(100 μmol/L).H2C9 cellswere divided into control,HG+Pal+Ole,HG+Pal+Ole+NaHS and Pal+Ole+DJ-1 siRNA+NaHS groups.The protein level of Mfn2,Fis1,CSE,and DJ-1 was determined by Western blot.Mitotracker staining was used to observe the morphology of mitochondria.The ultra-structural alteration of cardiac tissues was detected by transmission electron microscopy.The cardiac functions were detected by echocardiography.Results Expression of Fis1 was increased(P＜0.05)and expression of Mfn2 was decreased(P＜0.05)in db/db and H9C2 treated by HG+Pal+Ole compared to control group.NaHS could upregulate the expression DJ-1,enhance the expression of Mfn2,and reduce the expression of Fis1.In db/db mice,cardiac systolic function was reduced.Disordered arrangement of myofilament,loss of cristae and mitochondrial fission were observed.NaHS could ameliorate these alterations.Conclusions NaHS may alleviate mitochondria injury by promoting mitochondrial fusion.