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目的探讨碳纳米管暴露致大鼠主动脉血管内皮损伤作用的机制。方法通过气管滴注染毒Wistar大鼠,观察不同剂量(0,3.5,17.5 mg/kg)和不同时间(7 d和30 d)的碳纳米管暴露后大鼠血清中氧化应激指标谷胱甘肽(GSH)、超氧阴离子(O_2~-·)的变化水平;利用酶联免疫吸附方法测定血清中可溶性血管细胞粘附分子-1(sICAM-1)和可溶性细胞间粘附分子-1(sVCAM-1)的表达水平;利用免疫组织化学方法观察主动脉血管内皮中血管细胞粘附分子-1(ICAM-1)和细胞间粘附分子-1(VCAM-1)的表达水平,同时采用粒径相当的纳米碳黑作为阴性对照和二氧化硅作为阳性对照。结果碳纳米管染毒组机体发生氧化应激,而且在一定范围内存在剂量和时间依赖关系;血清中sICAM-1、sVCAM-以及主动脉血管内皮ICAM-1和VCAM-1均有不同程度的过度表达,随着染毒剂量和染毒时间的增加而升高;与对照组比较,碳纳米管暴露组机体氧化损伤更为严重。结论碳纳米管暴露致机体发生氧化应激进而诱导细胞粘附分子ICAM-1和VCAM-1的表达,使血管内皮功能发生紊乱,促进动脉粥样硬化的形成。
Objective To investigate the mechanism of vascular endothelial injury induced by carbon nanotube (CNT) in rats. Methods The Wistar rats were instilled by tracheal instillation and the oxidative stress indexes such as glutathione (SICAM-1) and soluble intercellular adhesion molecule-1 (sICAM-1) were measured by enzyme linked immunosorbent assay (ELISA) (sVCAM-1) was detected by immunohistochemistry. The expression of vascular cell adhesion molecule-1 (ICAM-1) and intercellular adhesion molecule-1 (VCAM-1) in aortic endothelium was observed by immunohistochemistry Nano-carbon black with comparable particle size was used as a negative control and silica as a positive control. Results The carbon nanotubes exposed to oxidative stress, and there is a dose-dependent and time-dependent manner in a certain range; serum sICAM-1, sVCAM- and aortic vascular endothelium ICAM-1 and VCAM-1 have varying degrees of Overexpression increased with the increase of exposure dose and exposure time. Compared with the control group, the oxidative damage was more serious in the exposed group of carbon nanotubes. Conclusion Exposure to carbon nanotubes causes oxidative stress in the body and induces the expression of ICAM-1 and VCAM-1, which may lead to disorder of vascular endothelial function and promote the formation of atherosclerosis.