赵浩茜,邹慧玲,胡 芳.有氧运动抑制自发性高血压大鼠心肌中HMGB1/TLR4炎症通路[J].现代生物医学进展英文版,2018,(19):3633-3636. |
有氧运动抑制自发性高血压大鼠心肌中HMGB1/TLR4炎症通路 |
Aerobic Exercise Training Inhibits Cardiac HMGB1/TLR4 Pathway in Spontaneously Hypertensive Rats |
Received:March 21, 2018 Revised:April 18, 2018 |
DOI:10.13241/j.cnki.pmb.2018.19.007 |
中文关键词: 有氧运动 自发性高血压大鼠 高迁移率族蛋白1 Toll样受体4 心肌纤维化 |
英文关键词: Aerobic exercise Spontaneously hypertensive rats High mobility group box-1 protein Toll like receptor 4 Cardiac fibrosis |
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中文摘要: |
摘要 目的:探讨有氧运动对自发性高血压大鼠心肌中高迁移率族蛋白1 (high mobility group box-1 protein, HMGB1)/Toll样受体4(toll like receptor 4,TLR4)炎症通路的影响。方法:成年雄性大鼠分为三组:同源正常血压大鼠(Wistar-Kyoto rats,WKY),自发性高血压大鼠(spontaneoully hypertensive rat, SHR),自发性高血压大鼠运动组(SHR + exercise,SHR+EX)。运动为中等强度跑台运动,自制跑台,倾斜角设置为10度,运动强度逐步增强,持续12周。尾动脉检测血压,收集左心室,Masson染色检测心肌组织纤维化水平,RT-PCR法检测心肌中纤维化相关基因的mRNA水平,ELISA法检测炎症因子白介素6(Interleukin 6, IL-6)和肿瘤坏死因子α(tumor necrosis factor alpha, TNF-α)的蛋白水平,Western blot法检测HMGB1和TLR4的蛋白表达。结果:有氧运动可以明显降低SHR大鼠心肌中HMGB1(P<0.05)和TLR4(P<0.05)的蛋白表达以及炎症因子IL-6(P<0.05)和TNF-α(P<0.05)的蛋白水平。经过的有氧运动之后,SHR大鼠的体重(P<0.05)、收缩压(P<0.05)、舒张压明显降低(P<0.05);心肌纤维化水平和心肌中I型胶原(P<0.05)、转化生长因子-β(transforming growth factor-β,TGF-β,P<0.05)、α平滑肌肌动蛋白(α-smooth muscle actin,α-SMA,P<0.05)的mRNA水平出现显著下降。结论:有氧运动可抑制自发性高血压大鼠心肌中HMGB1/TLR4炎症通路。 |
英文摘要: |
ABSTRACT Objective: To investigate the role of high mobility group box-1 protein (HMGB1)/toll like receptor 4 (TLR4) pathway in exercise-induced attenuation of cardiac fibrosis in spontaneously hypertensive rats (SHR). Methods: The adult male SHR were divided into three groups as follows: (1) normotensive Wistar-Kyoto rats (WKY); spontaneously hypertensive rats (SHR); (3) SHR received exer- cise (SHR+EX). The aerobic exercise training on treadmill with an incline of 10 degrees was performed for 12 weeks. The intensity of the exercise training was moderate. Twenty-four hours after the last training session, blood pressure was measured, the left ventricles were removed for morphometric analysis, RT-PCR analysis, ELISA and Western blot analysis. Results: In this work, exercise training in SHR suppressed protein expression of HMGB1(P<0.05) and TLR4 (P<0.05), and reduced protein levels of inflammatory cytokines including interleukin 6 (IL-6, P<0.05) and tumor necrosis factor alpha (TNF-α, P<0.05) in myocardium. Furthermore, aerobic exercise training in SHR reduced blood pressure(P<0.05) and body weight (P<0.05), and effectively attenuated fibrosis (P<0.05) and reduced mRNA expres- sion of fibrosis-related proteins including Collagen-I (P<0.05), transforming growth factor-β(TGF-β, P<0.05), and α-smooth muscle actin (α-SMA, P<0.05) in myocardium. Conclusion: Aerobic exercise training ameliorated fibrosis and inflammation in myocardium of SHR, possibly via suppressing HMGB1/TLR4 pathway. |
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