ObjectiveTo investigate the possible mechanism of docosahexaenoic acid(DHA) regulating collagen expression by affecting the P38 MAPK pathway to play an anti-atrial fibrillation.
MethodsEighty SD rats sensitive to acetylcholine(66 μg/mL)-calcium chloride(50 mg/mL) mixture were randomly divided into the control group(CON group), control DHA treatment group(DHA group), atrial fibrillation group(AF group) and atrial fibrillation DHA treatment group(DHA+AF group)(20 rats in each group model of atrial fibrillation).The BL-420F tractive electrocardiogram and continuous double stimulation method were used to detect the atrial effective refractory period(ERP), the whole cell patch clamp technique was used to record the atrial muscle cell action potential duration(APD) change, the enzyme immunosorbent assay(ELISA) was used to detect the typeⅠ, Ⅲ collagen expression in atrial muscle tissue of rats, and the expression levels of P38 and P-PP38 and MKP 1 protein were detected using Western blotting.
ResultsThe duration of atrial fibrillation in rats prolonged with the increasing of experimental time, while DHA could shorten the duration of atrial fibrillation(P < 0.05 to P < 0.01).The ERP and APD significantly shortened, while DHA could significantly prolong the atrial ERP and APD in AF group(P < 0.01).There was no significant change in P38 protein among each group.Compared with the CON group, the expression level of P-P38 significantly increased, while the expression level of MKP-1 decreased in AF group(P < 0.01). Compared with the AF group, the expression level of P-P38 significantly decreased, while the expression level of MKP-1 increased in the DHA+AF group(P < 0.01).The results of ELISA showed that DHA could obviously down-regulate the typeⅠand Ⅲ collagen expression(P < 0.01).
ConclusionsDHA may play an anti-atrial fibrillation role by regulating P38 MAPK signal transduction pathway mediating collagen expression.
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