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目的研究蝇蛆壳聚糖(HMC)对过氧化氢(H2O2)诱导的内皮细胞氧化应激损伤的保护作用。方法利用H2O2诱导的内皮细胞损伤模型,采用不同剂量HMC预培养,通过四甲基偶氮噻唑蓝(MTT)比色法检测细胞存活率,生化法和放免法检测细胞培养液超氧化物歧化酶(SOD)和丙二醛(MDA)、一氧化氮(NO)和内皮素(ET)水平。结果中、高剂量HMC组细胞存活率A值分别为(0.714 0±0.059 5)、(0.811 9±0.059 7),均高于H2O2损伤组(0.597 2±0.042 2)(P<0.01);低、中、高剂量HMC组细胞SOD活性分别为(14.76±1.59)、(16.99±1.69)、(19.22±2.31)NU/mL,明显高于H2O2损伤组(P<0.05,P<0.01);低、中、高剂量HMC组细胞MDA含量分别为(10.11±1.91)、(8.23±1.64)、(6.74±1.26)nmol/L,明显低于H2O2损伤组(P<0.01);各剂量HMC组细胞NO水平明显高于H2O2损伤组,而ET含量则明显低于H2O2损伤组(P<0.01)。结论 HMC具有保护血管内皮细胞的作用,机制可能与减少细胞NO释放、增加ET水平、维护内皮细胞结构和功能完整及增强其抗氧化能力有关。
Objective To study the protective effect of fly maggot chitosan (HMC) on oxidative stress induced by hydrogen peroxide (H2O2) in endothelial cells. Methods HUVEC-induced endothelial cell injury model was pretreated with different doses of HMC. Cell viability was measured by MTT colorimetric assay. The levels of superoxide dismutase (SOD), malondialdehyde (MDA), nitric oxide (NO) and endothelin (ET). Results The cell viability values of medium and high dose HMC groups were (0.714 0 ± 0.059 5) and (0.811 9 ± 0.059 7), respectively, which were higher than that of H2O2 injury group (0.597 2 ± 0.042 2) (P <0.01) (14.76 ± 1.59), (16.99 ± 1.69) and (19.22 ± 2.31) NU / mL respectively, which were significantly higher than those in H2O2-injured group (P <0.05, P <0.01) (10.11 ± 1.91), (8.23 ± 1.64) and (6.74 ± 1.26) nmol / L respectively, which were significantly lower than those in H 2 O 2 -induced group (P <0.01) NO level was significantly higher than that of H2O2 injury group, while ET content was significantly lower than H2O2 injury group (P <0.01). Conclusion HMC has protective effect on vascular endothelial cells. The mechanism may be related to the reduction of NO release, ET, the maintenance of endothelial cell structure and function, and the enhancement of its antioxidant capacity.