代谢性疾病中巨噬细胞极化的机制及运动对其调控作用的研究进展

Advance of effect of exercise on macrophage polarization in metabolic diseases and its potential mechanism

本文综述了运动对代谢性疾病中巨噬细胞极化的影响及其发挥作用的可能机制。近年来,巨噬细胞极化以其在代谢性疾病中的重要调控作用而在运动科学研究领域备受关注。随着研究的深入,发现不同方式运动均可通过增加巨噬细胞M2型极化产生抗炎效应以改善机体代谢,促进健康。因此,运动作为防治代谢性疾病的有效手段,其促进健康的机制可能与促进巨噬细胞M2型极化有关。可能的调控机制如下:①运动通过抑制TLR4活性、下调NF-κB信号下调TLR通路,减少巨噬细胞M1型极化;②运动通过改善肥胖下调JNK通路,抑制巨噬细胞M1型极化;③运动通过增加机体IL-13和IL-4分泌促进AMPK磷酸化、PPAR激活、SCOS1表达并抑制SCOS3表达激活AMPK通路、JAK/STAT通路和PI3K/AKT通路以促进巨噬细胞M2型极化。综上,运动可通过调节多条信号通路发挥促进巨噬细胞M2型极化并抑制M1型极化作用,这可能是运动改善机体代谢以促进健康的途径之一。

This study elaborates the effect of exercise on macrophage polarization in metabolic diseases and its possible mechanism.In recent years,macrophage polarization has attracted much attention in field of sports science due to its important regulatory role in metabolic diseases.With the deepening of research,it was found that exercise in different ways can improve metabolism and health by increasing M2 polarization of macrophages and producing anti-inflammatory effects.Therefore,as an effective means to prevent and treat metabolic diseases,mechanism of exercise promoting health may be related to promoting macrophage M2 polarization.Specific regulatory mechanisms are as follows:①Exercise reduces M1 polarization by down-regulating TLR4 and NF-κB signal to inhibit TLR pathway;②Exercise reduces JNK pathway to inhibit M1 polarization in obesity;③Exercise increases AMPK phosphorylation,PPAR activation,SCOS-1 contain and decrease SCOS-3 contain by increasing IL-13 and IL-4 secretion to improve AMPK pathway,JAK/STAT pathway and PI3K/AKT pathway,to promote M2 polarization.In conclusion,exercise can promote macrophage M2 polarization and inhibit M1 polarization by regulating multiple signaling pathways,which may be one of its way to improve metabolism and promote health.