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Insulin ameliorates myocardial inflammation and promotes recovery of T cell in murine experimental autoimmune myocarditis
Author(s) -
Zhang Yuan,
Zhuang Ran,
Geng Chaoqun,
Tian Na,
Cai Xiaoqing,
Lei Wen,
Gao Feng
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.680.22
Subject(s) - insulin , medicine , inflammation , endocrinology , myocarditis
Aim Glucose‐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. Methods BALB/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. Results Insulin 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. Conclusions These 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)