炎症反应与肌肉减少症

Inflammation and sarcopenia

肌肉减少症作为一种慢性增龄疾病,其发病率与人口老龄化密切相关,其发病机制复杂多样。炎症反应作为人类机体一种重要的免疫防御机制,有助于机体抵抗病原微生物感染,但炎症反应失调也会导致组织器官损伤,从而促使疾病发生。当机体发生炎症反应时会释放出炎症因子如肿瘤坏死因子-α(tumor necrosis factor-alpha,TNF-α)、白介素-1β(interleukin-1 beta,IL-1β)、白介素-6 (interleukin-6,IL-6)、转化生长因子-β(transforming growth factor-beta, TGF-β)、白介素-8 (interleukin-8,IL-8)等,若炎症因子在骨骼肌过多积累会导致肌肉萎缩,从而导致肌肉减少症的发生。其中活性氧形成激活核因子kappaB(nuclear factor kappa-B,NF-κB)通路,释放炎症因子如环氧合酶-2 (coclooxygenase-2,COX-2)、一氧化氮合成酶-2 (nitric oxide synthase-2,NOS-2)、TNF-α、IL-1β等,诱发炎症反应导致肌肉萎缩的机制尤其受到国内外研究人员的关注。但对于炎症作用造成肌肉减少症的具体机制研究很少,本文对此进行综述。

As a chronic aging disease,sarcopenia is closely related to population aging,and its pathogenesis is complex and diverse.As an important immune defense mechanism of human body,inflammatory response is helpful for the body to resist pathogen microbial infection,but the imbalance of inflammatory response can also lead to tissue and organ damage,thus promoting the occurrence of disease.Inflammatory factors such as tumor necrosis factor-alpha(TNF-α),interleukin-1 beta(IL-1β),interleukin-6(IL-6),transforming growth factor-beta(TGF-β),interleukin-8(IL-8),etc.,are released when the body has inflammatory reactions.Excessive accumulation of inflammatory factors in skeletal muscle will lead to muscle atrophy,leading to the occurrence of sarcopenia.Among them,reactive oxygen forms and activates the nuclear factor kappa-B(NF-κB)pathway,releasing inflammatory factors such as coclooxygenase-2(COX2),nitric oxide synthase-2(NOS-2),TNF-α,IL-1β,etc.,and the mechanism of inducing inflammatory response leading to muscle atrophy has been particularly concerned by researchers at home and abroad.However,there are few studies on the specific mechanism of inflammation causing sarcopenia.This article reviews the mechanism of inflammation and sarcopenia.