有氧运动通过Sestrin1蛋白抑制动脉粥样硬化中的炎症反应

IF 3.3 3区 医学 Q2 GERIATRICS & GERONTOLOGY Experimental Gerontology Pub Date : 2021-06-15 DOI:10.21203/RS.3.RS-592550/V1
Yunfeng Sun, Yawei Wu, Yingping Jiang, Hao Liu
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引用次数: 10

摘要

有氧运动在预防和治疗动脉粥样硬化中具有重要作用。炎症反应是动脉粥样硬化发生发展阶段的主要病理过程。sesn被认为是动脉粥样硬化中的抗炎症蛋白。本研究发现有氧运动条件下SESN1表达水平较高,进一步研究发现与未进行有氧运动的动脉粥样硬化小鼠相比,其IL-1β/IL-6/TNF-α水平明显受到抑制。此外,我们发现NF-κB信号的激活受到阻碍。结合我们前期的研究,SESN1被认为是有氧运动的下游因子,往往会抑制炎症信号的激活,从而抑制炎症因子的表达水平。另一个令人兴奋的发现是MMP9/13也受到抑制,但潜在的机制尚不清楚。总的来说,本研究通过SESN1揭示了有氧运动对炎症和斑块稳定性的重要性,可能有助于开发新的动脉粥样硬化临床治疗方法。
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Aerobic exercise inhibits inflammatory response in atherosclerosis via Sestrin1 protein
Aerobic exercise plays an important role in prevention and treatment of atherosclerosis. Inflammatory response is the main pathological process during occurrence and development stage of atherosclerosis. SESNs are considered as anti-inflammation protein in atherosclerosis. In current study, a high expression level of SESN1 is identified under the condition of aerobic exercise, further investigation shows levels of IL-1β/IL-6/TNF-α are significantly suppressed compared to those atherosclerosis mice with no aerobic training. Besides, we find that the activation of NF-κB signaling is impeded. Combine with our previous study, SESN1 is considered as the downstream factor of aerobic exercise which tend to inhibit the activation of inflammatory signaling and result in suppress the expression level of inflammatory factors. Another exciting finding is that MMP9/13 are also suppressed,but the potential mechanism is unclear. Overall, present study sheds light on the significance of aerobic exercise for inflammation and stability of plaque through SESN1 may help developing new clinical treatments of atherosclerosis.
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来源期刊
Experimental Gerontology
Experimental Gerontology 医学-老年医学
CiteScore
7.30
自引率
2.60%
发文量
280
审稿时长
1 months
期刊介绍: Experimental Gerontology is a multidisciplinary journal for the publication of work from all areas of biogerontology, with an emphasis on studies focused at the systems level of investigation, such as whole organisms (e.g. invertebrate genetic models), immune, endocrine and cellular systems, as well as whole population studies (e.g. epidemiology). The journal also publishes studies into the behavioural and cognitive consequences of aging, where a clear biological causal link is implicated. Studies aimed at bridging the gap between basic and clinical aspects of gerontology, such as papers on the basic aspects of age-related diseases, are welcomed, as is research orientated toward the modulation of the aging process. Original research manuscripts, special issues, short reports, reviews, mini-reviews, and correspondence are published. Manuscripts on social aspects of aging and reports on clinical studies do not fall within the scope of the journal.
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