Abstract
AimGlucose‐insulin‐potassium is a useful adjunct to myocarditis. Besides its essential action in energy metabolism, insulin also exerts an anti‐inflammatory effect. This study investigated the effect of insulin on myocardial inflammation in experimental autoimmune myocarditis (EAM) mice and its underlying mechanisms.MethodsBALB/c mice were immunized subcutaneously with myocarditogenic peptide MyHC‐a and randomly divided into mock‐immunized, saline‐treated and insulin‐treated groups. T lymphoma cell line EL4 was used for in vitro study.ResultsInsulin reduced pro‐inflammatory cytokine IL‐1β with no changes of blood glucose and autoantibody production. Inflammatory infiltrates were less abundant in insulin‐treated hearts than those in saline‐treated hearts on day 21 after immunization. Meanwhile, insulin significantly reduced sera cTnI of EAM mice on day 14 and 21 (P<0.05). Interestingly, insulin promoted T cell recovery. CD3+ T cells in insulin‐treated mice proliferated more vigorously than those in saline‐treated mice without changing the memory/naïve T cell ratio. Moreover, ERK1/2 inhibitors blocked the insulin‐induced EL4 cells proliferation.ConclusionsThese data suggest that insulin exerts an anti‐inflammatory action in EAM and increases T cell proliferation by activating ERK1/2.Supported by the State Key Program of National Natural Science Foundation of China (No. 81030005)
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call