Background The occurrence and development of atrial fibrillation is complex. A large number of studies have shown that oxidative stress is closely related to atrial fibrillation. Apocynin (APO) is an important oxidase inhibitor in the process of oxidative stress injury, which can resist oxidative stress injury.
Objective To study the protective effect of apocynin on L-type calcium current (ICa,L) and action potential duration (APD) in rabbit left atrial myocytes under oxidative stress injury.
Methods We used enzyme to get single left atrial myocytes of rabbit, and they were divided into control group (n=13), H2O2(10 μmol/L) group (n=13), H2O2 (50 μmol/L) group (n=13), H2O2 (50 μmol/L) + APO (100 μmol/L) group, APO (100 μmol/L) group (n=13). The whole cell patch clamp technique was used to study the protective effect of APO on ICa,L and APD under oxidative stress injury. Real-time qPCR and Western blot were used to detect the expression of CACNA1C mRNA and CaV1.2 protein levels.
Results In the H2O2 (10 μmol/L) group, the peak value of ICa,L declined from (−18.5±0.1) pA/pF to (−10.7±0.7) pA/pF (P<0.01); In the H2O2 (50 μmol/L) group, the peak value of ICa,L declined from (−18.5±0.1) pA/pF to (−9.4±0.8) pA/pF (P<0.01); In H2O2 (50 μmol/L) + APO (100 μmol/L) group, the peak value of ICa,L was (−16.7±1.6) pA/pF, significantly higher than that in the H2O2 (50 μmol/L) group after treatment (P<0.01); In APO (100 μmol/L) group, the peak of ICa,L was (−17.2±1.3) pA/pF, similar to the control group (P>0.01). APO also recovered the shortened APD50 induced by H2O2. Compared with H2O2 group, the expression of CACNA1C mRNA and the protein levels of CaV1.2 decreased (P<0.05), which could be recovered by APO.
Conclusion APO have the protective effect on ICa,Land APD in left atrial myocytes of rabbit.