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[目的]探讨枸杞多糖组分-Ⅳ(LBP-Ⅳ)对对氧磷(PARA)所致血管内皮功能损伤的保护作用及其机制。[方法]以大鼠离体胸主动脉血管环(EVAPVR)和培养的人脐静脉内皮细胞(HUVEC)为试验对象,以PARA为损伤药物,以LBP-Ⅳ为保护药,检测血管内皮依赖性舒张反应(EDRR)、内皮细胞单层通透性(ECMP)及细胞培养液生化指标。[结果]LBP-Ⅳ剂量依赖性(0.1、1、10mg/ml)地显著减轻了PARA(3.63μmol/L)对血管EDRR的抑制作用,降低了ECMP的增加,保护了超氧化物歧化酶(SOD)活性,阻滞了丙二醛(MDA)浓度的升高以及一氧化氮(NO)浓度的降低(P<0.05)。[结论]LBP-Ⅳ对PARA所致的血管内皮功能损伤有明显的保护作用,其机制可能与LBP-Ⅳ的抗氧化作用有关。
[Objective] To investigate the protective effect of LBP-Ⅳ on vascular endothelial dysfunction induced by paraoxon-phosphorylation (PARA) and its mechanism. [Methods] Rat isolated thoracic aortic vascular rings (EVAPVR) and cultured human umbilical vein endothelial cells (HUVEC) were used as experimental subjects. PARA was used as an injury drug and LBP-Ⅳ as a protective drug to detect endothelium-dependent Relaxation response (EDRR), endothelial cell monolayer permeability (ECMP) and cell culture medium biochemical indicators. [Results] LBP-IV significantly reduced the inhibitory effect of PARA (3.63μmol / L) on the vascular endothelial growth factor receptor (EDRR), reduced the increase of ECMP and protected the activity of superoxide dismutase SOD activity, blocked the increase of malondialdehyde (MDA) concentration and the decrease of nitric oxide (NO) concentration (P <0.05). [Conclusion] LBP-IV can protect PARA-induced endothelial dysfunction and its mechanism may be related to the anti-oxidative effect of LBP-IV.