Zhou M, Chen Y, Ouyang Q, Liu S, Pang Z J, Wan J
Research Laboratory of Free Radical Medicine, First Military Medical University, Guangzhou, China.
Am J Chin Med. 1998;26(3-4):301-10. doi: 10.1142/S0192415X98000348.
Our previous studies have shown that a protein-bound polysaccharide, polysaccharide krestin (PSK), can protect macrophages from lipoperoxidative injury induced by tert-butyl hydroperoxide (tbOOH) and oxidatively modified low density lipoprotein (O-LDL). PSK was administered intraperitoneally to mice, and the peritoneal macrophages harvested were used as an experimental model. PSK does not reveal any protective effect on macrophages injured by tbOOH when incubated in vitro. In order to elucidate its mode of action, in the present study, the protective effects of PSK were further investigated using morphological changes and viability as indices. It was shown that, compared with the non-PSK group, the viability of macrophages was much higher in the PSK group, and the morphological changes in the PSK group were much less than those in the non-PSK group. The protective effect of PSK administered intraperitoneally and orally on macrophages injured by tbOOH was comparable. Furthermore, the serum of the PSK treated mice had the same protective effect.
我们之前的研究表明,一种蛋白结合多糖,裂褶菌多糖(PSK),可以保护巨噬细胞免受叔丁基过氧化氢(tbOOH)和氧化修饰低密度脂蛋白(O-LDL)诱导的脂质过氧化损伤。将PSK腹腔注射给小鼠,收获的腹腔巨噬细胞用作实验模型。在体外培养时,PSK对受tbOOH损伤的巨噬细胞没有显示出任何保护作用。为了阐明其作用方式,在本研究中,以形态变化和活力为指标进一步研究了PSK的保护作用。结果表明,与非PSK组相比,PSK组巨噬细胞的活力要高得多,且PSK组的形态变化比非PSK组少得多。腹腔注射和口服PSK对受tbOOH损伤的巨噬细胞的保护作用相当。此外,PSK处理小鼠的血清具有相同的保护作用。