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

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...

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

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.