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林产化学与工业

林产化学与工业 ›› 2013, Vol. 33 ›› Issue (1): 45-48.doi: 10.3969/j.issn.0253-2417.2013.01.008

• 1研究报告 • 上一篇    下一篇

松针叶绿素-胡萝卜素软膏体外抗脂质过氧化作用的研究

郑光耀1, 何玲2, 薄采颖1, 谢衡3, 刘冬芹2, 李若达3   

  1. 1. 中国林业科学研究院 林产化学工业研究所;生物质化学利用国家工程实验室;国家林业局 林产化学工程重点开放性实验室, 江苏 南京 210042;2. 中国药科大学 药理学教研室, 江苏 南京 210009;3. 中健行集团有限公司, 广东 乐昌 512229
  • 收稿日期:2012-06-28 修回日期:1900-01-01 出版日期:2013-02-28 发布日期:2013-02-28

Anti-lipid Peroxidation of Chlorophyll-carotene Paste from Pine Needles in Vitro

ZHENG Guang-yao1, HE Ling2, BO Cai-ying1, XIE Heng3, LIU Dong-qin2, LI Ruo-da3   

  1. 1. Institute of Chemical Industry of Forest Products, CAF;National Engineering Lab. for Biomass Chemical Utilization;Key and Open Lab. of Forest Chemical Engineering, SFA, Nanjing 210042, China;2. Department of Pharmacology, China Pharmaceutical University, Nanjing 210009, China;3. Zhongjianxing Group Corporation Limited, Lechang 512229, China
  • Received:2012-06-28 Revised:1900-01-01 Online:2013-02-28 Published:2013-02-28

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摘要： 探讨松针叶绿素-胡萝卜素软膏的体外抗脂质过氧化作用,在大鼠肝匀浆和肝线粒体中加入不同浓度的松针叶绿素-胡萝卜素软膏,观察它们对大鼠肝匀浆自发性过氧化、VC-Fe2+诱导肝匀浆和肝线粒体脂质过氧化的丙二醛(MDA)抑制效果。结果表明:松针叶绿素-胡萝卜素软膏能有效抑制大鼠肝匀浆的自发性和诱导性脂质过氧化产生的MDA,其抑制率为50%时药物浓度(IC50)分别为398.72和355.05 mg/L,对肝线粒体的诱导性脂质过氧化产生的MDA也有较好的抑制作用,其IC50为687.02 mg/L,还能减轻肝线粒体的肿胀程度,且呈现良好的量效关系。

关键词: 松针, 提取物, 肝匀浆, 线粒体, 脂质过氧化

Abstract: Anti-lipid peroxidation of chlorophyll-carotene paste from pine needles was investigated in vitro. MDA production in rat liver homogenate and mitochondria spontaneously formed or induced by VC-Fe2+ system were measured. The results showed that the chlorophyll-carotene paste could inhibit the generation of MDA in liver homogenate under spontaneous and induced conditions, as well as in liver mitochondria under induced condition, with IC50 of 398.72 mg/L, 355.05 mg/L and 687.02 mg/L, respectively. The swelling of liver mitochondria was also inhibited with dose-response relationship. It is suggested that chlorophyll-carotene paste from pine needles possessed anti-oxidant activity in vitro.

Key words: pine needles, extract, liver homogenate, mitochondria, lipid peroxidation

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