壳寡糖弱化过氧化氢介导的内皮细胞损伤

                                                          译者：乔莹

H.-T. Liu, W.-M. Li, G. Xu, X.-Y. Li, X.-F. Bai, P. Wei, C. Yu, and Y.-G. Du, Chitosan oligosaccharides attenuate hydrogen peroxide-induced stress injury in human umbilical vein endothelial cells. Pharmacological Research 59 (2009) 167-175.
    中国科学院大连化学物理研究所杜昱光研究员所领导的研究小组一直致力于壳寡糖的应用研发工作，发表英文论文20余篇。该研究组最新成果发表在Pharmacological Research上，研究发现壳寡糖可以弱化过氧化氢介导的内皮细胞损伤。
    壳寡糖的抗肿瘤，免疫增强及抑菌活性很早前就有报道，而更多的生物学活性还有待开发。这篇文章中，作者发现壳寡糖可以保护内皮细胞的氧化性损伤。经过24小时的壳寡糖预处理，过氧化氢诱导的细胞损伤明显减少。这种弱化效果与显著降低胞内活性氧的产生密切相关。壳寡糖还可以显著抑制脂质过氧化反应，调控胞内抗氧化酶(SOD)和(GSH-Px)活性。增加胞内一氧化氮的产生，并且降低过氧化氢诱导的细胞凋亡。
Chitosan oligosaccharides (COS) have been reported to have anticancer activity, immuno-enhancing effect and antimicrobial activity. However, other biological activities are unknown. Herein, we investigated the protective effects of COS against hydrogen peroxide (H2O2)-induced oxidative damage on human umbilical vein endothelial cells (HUVEC, ECV304 cells). After 24 h pre-incubation with COS (25–200ug/ml), the viability loss in ECV304 cells induced by H2O2 (300uM) for 12 h was markedly restored in a concentration dependent manner as measured by MTT assay. This effect was accompanied by a marked decrease in intracellular reactive oxygen species (ROS) by measuring intensity of DCFH fluorescence. COS also exerted preventive effects on suppressing the production of lipid peroxidation such as malondialdehyde (MDA), restoring activities of endogenous antioxidants including superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), along with the capacity of increasing levels of nitric oxide (NO) and nitric oxide synthase (NOS), as were determined by commercial regent kits. In addition, pre-incubation of COS with ECV304 cells for 24 h resulted in the reduction of apoptosis and the induction of cell cycle arrest in G1/S+M phase as assayed quantitatively by Annexin V-fluorescein isothiocyanate (FITC) apoptosis detection kit using flow cytometry. Taken together, our findings suggest that COS can effectively protect HUVECs against oxidative stress by H2O2, which might be of importance in the treatment of cardiovascular diseases.