Pang Z J, Zhou M, Chen Y, Wan J
Research Laboratory of Free Radical Medicine, First Military Medical University, Gaungzhou, China.
Am J Chin Med. 1998;26(2):133-41. doi: 10.1142/S0192415X9800018X.
The aim of this study is to examine whether polysaccharide krestin, a protein-bound polysaccharide, can prevent the progression of atherosclerosis and lipoperoxidative injury caused by oxidatively modified low density lipoprotein (Ox-LDL) to macrophages. The alterations of GSHPx (glutathione peroxidase), SOD (superoxide dismutase) activity and NO (nitric oxide) release in PSK-treated mouse peritoneal macrophages, and the effect of LPS on them were investigated. With peritoneal injection of PSK, the following were observed in the mouse peritoneal macrophages: 1) an increase in SeGSHPx activity, 2) elevation in non-SeGSHPx and SOD activity; 3) the enzyme activities were further improved by addition of lipopolysaccharide (LPS); and 4) much NO was found to be released by PSK-treated mouse peritoneal macrophages stimulated by LPS.
本研究的目的是检验裂褶菌多糖（一种蛋白结合多糖）是否能够预防动脉粥样硬化的进展以及氧化修饰低密度脂蛋白（Ox-LDL）对巨噬细胞造成的脂质过氧化损伤。研究了经裂褶菌多糖处理的小鼠腹腔巨噬细胞中谷胱甘肽过氧化物酶（GSHPx）、超氧化物歧化酶（SOD）活性以及一氧化氮（NO）释放的变化，以及脂多糖对它们的影响。通过腹腔注射裂褶菌多糖，在小鼠腹腔巨噬细胞中观察到以下情况：1）硒谷胱甘肽过氧化物酶（SeGSHPx）活性增加；2）非硒谷胱甘肽过氧化物酶和超氧化物歧化酶活性升高；3）添加脂多糖（LPS）后酶活性进一步提高；4）发现经裂褶菌多糖处理的小鼠腹腔巨噬细胞在受到LPS刺激时会释放大量NO。
