Daoying Xu1, Aiqin Wang2, Fengqin Jiang1, Junhong Hu1, Xiuzhou Zhang1. 1. Department of Cardiology, Binzhou People's Hospital Binzhou City 256610, Shandong Province, China. 2. Department of Critical Care Medicine, Binzhou People's Hospital Binzhou City 256610, Shandong Province, China.
Abstract
BACKGROUND: Interleukin-37 (IL-37) is a new discovered member of the interleukin family and plays anti-inflammatory effect in some inflammatory disease. A recent study found that IL-37 elevated significantly in peripheral blood of patients with acute myocardial infarction. We aimed to explore the effect IL-37 on cardiac function after mice myocardial infarction (MI) and its mechanism. METHODS: Acute MI mouse model was established and divided into three groups: sham group, MI group and IL-37 treatment group. MPO expression was detected by immunohistochemistry; NF-κB signaling pathway was tested by Western blot; and cardiac function was measured by echocardiography. RESULTS: Compared with MI mice, IL-37 treatment showed an obvious decrease of MPO expression, suppression of p-p65 expression, and improved cardiac function by decreasing left ventricular shortening fraction (LVFS). CONCLUSION: IL-37 may improve MI mice cardiac function via inhibition of inflammatory NF-κB signaling pathway.
BACKGROUND: Interleukin-37 (IL-37) is a new discovered member of the interleukin family and plays anti-inflammatory effect in some inflammatory disease. A recent study found that IL-37 elevated significantly in peripheral blood of patients with acute myocardial infarction. We aimed to explore the effect IL-37 on cardiac function after micemyocardial infarction (MI) and its mechanism. METHODS: Acute MI mouse model was established and divided into three groups: sham group, MI group and IL-37 treatment group. MPO expression was detected by immunohistochemistry; NF-κB signaling pathway was tested by Western blot; and cardiac function was measured by echocardiography. RESULTS: Compared with MI mice, IL-37 treatment showed an obvious decrease of MPO expression, suppression of p-p65 expression, and improved cardiac function by decreasing left ventricular shortening fraction (LVFS). CONCLUSION:IL-37 may improve MI mice cardiac function via inhibition of inflammatory NF-κB signaling pathway.
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