刘焕, 茹凝玉, 王忠超, 吕强, 白云刚, 董栋, 李少华, 马进. 间断人工重力在模拟失重所致胸主动脉炎症反应中的对抗作用[J]. 心脏杂志, 2021, 33(2): 186-191, 194. DOI: 10.12125/j.chj.202011003
    引用本文: 刘焕, 茹凝玉, 王忠超, 吕强, 白云刚, 董栋, 李少华, 马进. 间断人工重力在模拟失重所致胸主动脉炎症反应中的对抗作用[J]. 心脏杂志, 2021, 33(2): 186-191, 194. DOI: 10.12125/j.chj.202011003
    Huan LIU, Ning-yu RU, Zhong-chao WANG, Qiang LV, Yun-gang BAI, Dong DONG, Shao-hua LI, Jin MA. Intermittent artificial gravity prevents inflammatory response in thoracic aorta induced by simulated microgravity[J]. Chinese Heart Journal, 2021, 33(2): 186-191, 194. DOI: 10.12125/j.chj.202011003
    Citation: Huan LIU, Ning-yu RU, Zhong-chao WANG, Qiang LV, Yun-gang BAI, Dong DONG, Shao-hua LI, Jin MA. Intermittent artificial gravity prevents inflammatory response in thoracic aorta induced by simulated microgravity[J]. Chinese Heart Journal, 2021, 33(2): 186-191, 194. DOI: 10.12125/j.chj.202011003

    间断人工重力在模拟失重所致胸主动脉炎症反应中的对抗作用

    Intermittent artificial gravity prevents inflammatory response in thoracic aorta induced by simulated microgravity

    • 摘要:
        目的  观察模拟失重大鼠胸主动脉炎症反应变化以及间断人工重力对抗模拟失重所致变化的作用。
        方法  采用尾部悬吊方法建立模拟失重大鼠模型,将45只雄性Sprague-Dawley大鼠随机分为3组,每组15只(n = 15)。即对照(CON)组、4周尾部悬吊(HU)组和1 h/d间断人工重力(IAG)组。建模成功后,分离大鼠胸主动脉,通过En face免疫荧光染色和离体单核细胞粘附实验观察血管内皮的单核细胞浸润情况;通过蛋白免疫印迹实验、免疫组织化学染色观察血管细胞粘附分子1(VCAM-1)和单核细胞趋化蛋白1(MCP-1)的蛋白表达和定位;通过酶联免疫吸附实验观察肿瘤坏死因子α(TNF-α)、白介素(IL)-1β、IL-6的表达水平,通过实时定量PCR技术观察上述因子的mRNA表达水平。
        结果  与CON组比较,HU组大鼠胸主动脉内皮表面粘附的单核细胞和THP-1细胞数量显著增多(P<0.01),胸主动脉VCAM-1、MCP-1、TNF-α、IL-1β的蛋白和mRNA表达水平显著增加(P<0.01)。与HU组比较,IAG组大鼠胸主动脉内皮表面粘附的上述细胞数量显著降低(P<0.05或P<0.01),VCAM-1、MCP-1、TNF-α、IL-1β的蛋白和mRNA表达水平显著降低(P<0.05或P<0.01)。另外,胸主动脉IL-6的表达水平在三组间无显著统计学差异。
        结论  模拟失重引起大鼠胸主动脉发生炎症反应,此变化可通过IAG干预进行抑制,提示IAG可能通过抑制炎症反应对抗模拟失重所致胸主动脉重建过程。

       

      Abstract:
        AIM  To investigate inflammatory response in thoracic aorta induced by simulated microgravity and the protective effect of intermittent artificial gravity (IAG) on this change.
        METHODS  Hindlimb unloading (HU) rat model was used to simulate the effects of weightlessness on cardiovascular system. Forty-five male Sprague-Dawley rats were randomly divided into 3 groups (fifteen in each group): a control group (CON), a 4-week HU group (HU) and a 1 h/d IAG group (IAG). After successfully modeling, monocyte infiltration into the arterial wall of thoracic aorta was assessed by en-face immunofluorescence staining and in vitro monocyte binding assay. The protein expressions of vascular cell adhesion molecule 1 (VCAM-1) and monocyte chemoattractant protein 1 (MCP-1) were detected by Western blot analysis and immunohistochemistry. The expression levels of tumour necrosis factor α (TNF-α), interleukin (IL)-1β and IL-6 were examined by Enzyme-linked immunosorbent assay. The real-time polymerase chain reaction (PCR) was performed to measure the mRNA expressions of the above cytokines.
        RESULTS  The numbers of monocytes and THP-1 cells adhesion to endothelium as well as the protein and mRNA expressions of VCAM-1, MCP-1, TNF-α and IL-1β were significantly increased in HU rats. Compared with those in HU rats, there was a significant decrease in the numbers of monocytes and THP-1 cells binding to endothelium as well as the protein and mRNA expressions of VCAM-1, MCP-1, TNF-α and IL-1β in IAG rats. There was no difference in the expression of IL-6 among the three groups.
        CONCLUSION  Simulated microgravity results in inflammatory response in thoracic aorta, which is reversed by 1 h/G IAG. These results suggest that IAG may prevent simulated microgravity-induced arterial remodeling in thoracic aorta by inhibiting inflammatory response.

       

    /

    返回文章
    返回