壳聚糖及其低分子衍生物的细胞因子诱导和抗炎活性。

V N Davydova, A A Kalitnik, P A Markov, A V Volod'ko, S V Popov, I M Ermak
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引用次数: 0

摘要

获得了该多糖的低分子衍生物(5 kDa),并通过壳聚糖(110 kDa)的自由基解聚研究了其诱导细胞因子和抗炎活性。结果表明,高分子壳聚糖对内毒素诱导的抗炎细胞因子、肿瘤坏死因子α的合成有抑制作用。在经口引入实验动物的情况下,高分子和低分子壳聚糖刺激小鼠血清中抗炎细胞因子IL-10的合成;在这种情况下,高分子衍生物的活性比初始多糖高两倍。经口给药后,初始多糖(50 mg/kg)及其衍生物可抑制实验动物大肠化学诱导炎症的发展,表现为影响面积和对大肠壁的损伤程度减小,髓过氧化物酶活性降低2倍。根据形态学和生化特征,壳聚糖的作用与激素抗炎药强的松龙相似。
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[Cytokine-inducing and anti-inflammatory activity of chitosan and its low-molecular derivative].

A low-molecular derivative of the polysaccharide (5 kDa) was obtained and its cytokine-inducing and anti-inflammatory activity was studied by free radical depolymerization of chitosan (110 kDa). It was shown that high-molecular chitosan in vitro inhibited the synthesis of anti-inflammatory cytokine, the tumor necrosis factor alpha induced by endotoxin. In the case of peroral introduction to experimental animals, high- and low-molecular chitosans stimulated synthesis of the anti-inflammatory cytokine IL-10 in the blood serum of mice; in this case, the activity of the high-molecular derivative was two times higher as compared with the initial polysaccharide. With peroral introduction, the initial polysaccharide (50 mg/kg) and its derivative inhibited the development of chemically induced inflammation of experimental animals’ large intestines, which was manifested as a decrease in the affected area and the degree of damage to the large intestine wall, as well as a two-fold reduction of myeloperoxidase activity. According to morphological and biochemical characteristics, the effect of chitosans was similar to that of a hormone anti-inflammatory drug, prednisolone.

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