萼状粒毛盘菌多糖的生物活性

研究萼状粒毛盘菌YM-262胞内、胞外多糖对亚硝基的清除作用、对丙二醛生成的抑制作用、对线粒体的保护作用和抗炎作用。结果表明：胞内、胞外多糖质量浓度为1.2g·L-1时对亚硝酸盐的清除率可达最大,分别为63.21%和52.43%;胞内、胞外多糖均能显著抑制肝匀浆在自氧化和诱导氧化中丙二醛的生成,抑制率分别为32.81%和36.46%;此外,YM-262多糖可抑制.OH所致的氧化损伤,减轻线粒体膜肿胀度,且胞内多糖的抑制率大于胞外多糖;胞内多糖和胞外多糖均可显著抑制二甲苯所致的小鼠耳廓肿胀,减少左右耳质量差,且具有一定的剂量-效应关系,胞内多糖和胞外多糖剂量为400mg.kg-1时,抑制率分别为...

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Published in浙江大学学报（农业与生命科学版） Vol. 38; no. 4; pp. 524 - 528
Main Author 宋世玉 袁如月 孙柘 王平 蔡敬民 叶明
Format Journal Article
LanguageChinese
Published 合肥工业大学 生物与食品工程学院 ,安徽 合肥 230009%合肥学院 生物与环境工程系 ,安徽 合肥 230022 2012
Subjects
抗氧化作用
抗炎作用
胞内多糖
胞外多糖
萼状粒毛盘菌
抗氧化作用
萼状粒毛盘菌
胞内多糖
抗炎作用
胞外多糖
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ISSN1008-9209
DOI10.3785/j.issn.1008‐9209.2012.04.023

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Summary:研究萼状粒毛盘菌YM-262胞内、胞外多糖对亚硝基的清除作用、对丙二醛生成的抑制作用、对线粒体的保护作用和抗炎作用。结果表明：胞内、胞外多糖质量浓度为1.2g·L-1时对亚硝酸盐的清除率可达最大,分别为63.21%和52.43%;胞内、胞外多糖均能显著抑制肝匀浆在自氧化和诱导氧化中丙二醛的生成,抑制率分别为32.81%和36.46%;此外,YM-262多糖可抑制.OH所致的氧化损伤,减轻线粒体膜肿胀度,且胞内多糖的抑制率大于胞外多糖;胞内多糖和胞外多糖均可显著抑制二甲苯所致的小鼠耳廓肿胀,减少左右耳质量差,且具有一定的剂量-效应关系,胞内多糖和胞外多糖剂量为400mg.kg-1时,抑制率分别为56.68%和51.87%。
Bibliography:33-1247/S
Labhnum calyculiforme ; intracellular polysaccharide; extracellular polysaccharide;antioxidation; anti-inflammatory effect
The effects of intracellular polysaecharide （LIP） and extracellular polysaecharide （LEP） from Lachnum calyculiforme YM-262 on the elimination of nitrite radicals, the inhibition of MDA formation, the protective action of mitochondria, and the anti-inflammation were studied. The results indicated that the clearance rates of nitrite could reach 63.21H and 52：43H at 1.2 g-L-1 of LIP and LEP, respectively. LIP and LEP could significantly inhibit the amount of malondialdehyde which was produced by liver homogenate in the self-induced oxidation and the induced oxidation. The inhibition rate of malondialdehyde were 32.81% and 36.46% at 1.2 g. L-1 of LIP and LEP, respectively. In addition, polysaceharides from L. calyculiforme YM-262 could inhibit the oxidative damage made by - OH and reduce the swelling degree of mitochondrial membrane, and the LIP＇ s inhibitory rate was higher than the
ISSN:1008-9209
DOI:10.3785/j.issn.1008‐9209.2012.04.023