Effects of exercise training on inflammaging: the role of macrophages in the molecular mechanisms

运动训练可以阻止炎性巨噬细胞向脂肪组织的浸润，并对肥胖相关的慢性炎症具有抗炎作用。具有强抗炎作用的胃饥饿素在腹膜自噬细胞中的表达因肥胖而降低，并通过运动训练恢复，提示运动训练通过胃饥饿素抑制肥胖引起的炎症。另一方面，生物钟基因Rev-erb通过直接调节趋化因子Ccl2的表达来调节巨噬细胞的炎症功能。小鼠巨噬细胞系RAW264细胞过度表达Rev-erb抑制LPS内毒素刺激后Ccl2的诱导，导致细胞粘附和迁移活性受损。这些数据表明，Rev-erb通过抑制Ccl2表达调节巨噬细胞的炎症浸润，并参与衰老或肥胖相关的炎症。

Exercise training prevented the infiltration of inflammatory macrophages to adipose tissue and exerted anti-inflammatory effects for obesity-related chronic inflammation. Expression of ghrelin, which exerts potent anti-inflammatory effects, in peritoneal marophages was decreased by obesity and recovered by exercise training, suggesting that exercise training suppresses obesity-induced inflammation through ghrelin. On the other hand, a circadian clock gene Rev-erb modulates the inflammatory function of macrophages through the direct regulation of a chemokine Ccl2 expression. Overexpression of Rev-erb in murine macrophage cell line RAW264 cells suppressed the induction of Ccl2 following a LPS endotoxin challenge, resulting in impaired the activity of cell adhesion and migration. These data suggest that Rev-erb regulates the inflammatory infiltration of macrophages through the suppression of Ccl2 expression and participates in aging- or obesity-associated inflammation.