中国药物警戒 ›› 2013, Vol. 10 ›› Issue (9): 513-517.

• 基础与临床研究 •    下一篇

北豆根不同组分抗炎药效伴随毒副作用肝内损伤机制研究

栾永福12,孙蓉1*   

  1. 1.山东省中医药研究院,山东济南250014；
    2.天津中医药大学,天津300073
  • 收稿日期:2013-09-02 修回日期:2016-03-09 出版日期:2013-09-08 发布日期:2016-03-09
  • 通讯作者: 孙蓉,女,研究员·博导,博士,中药药理与毒理。 E-mail：sunrong107@163.com
  • 作者简介:栾永福,男,在读硕士,中药药理。
  • 基金资助:
    国家重点基础研究发展计划（973）中医基础理论专项资助项目课题（2009CB522802）。

Research of Liver Damage Mechanism of the Toxical and Side Effects Accompanied with Anti-inflammation Caused by Different Extracts from to Mice

LUAN Yong-fu1,2 ,SUN Rong1*   

  1. 1.Shandong Research Academy of TCM, Shandong Jinan 250014, China;
    2.Tianjin University of Traditional Chinese Medicine, Tianjin 300073, China
  • Received:2013-09-02 Revised:2016-03-09 Online:2013-09-08 Published:2016-03-09

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摘要： 目的 研究基于肝内过氧化损伤路径的北豆根水提、醇提组分在抗炎作用下伴随出现的毒副作用机制,为其“功效-毒性”相关性研究提供肝内物质水平变化的实验依据。方法建立复方巴豆油致小鼠耳肿胀模型和皮下注射琼脂致小鼠肉芽肿模型,分别给予不同剂量的北豆根水提组分、醇提组分连续灌胃3 天和7 天,末次给药后检测血清和肝组织内的超氧化物歧化酶（SOD）、丙二醛（MDA）、一氧化氮（NO）、一氧化氮合酶（NOS）、谷胱甘肽（GSH）、谷胱甘肽过氧化物酶（GSH-Px）的水平和活性。结果北豆根水提组分和醇提组分可使小鼠血和肝组织内MDA 含量增加,同时SOD 活性下降；血和肝组织中NO 含量增加,NOS 活性升高；血和肝组织中GSH 含量下降,GSH-Px 活性下降。上述变化趋势随剂量增加和时间延长而加重,与空白对照组有明显差异。结论北豆根水提、醇提组分对炎症小鼠产生的肝脏毒副作用机制可能与过氧化损伤机制有关。

关键词: 北豆根, 不同组分, 毒性, 肝内损伤机制, 氧化损伤

Abstract: Objective To research the mechanism based on liver oxidative damage path of the toxical and side effects accompanied with anti-inflammation of water and alcohol extract from . Thus, we try to provide experimental basis of intrahepatic material change for the study of correlation between toxicity and efficacy of Methods First, we made ear swelling model by compound recipe of croton oil and made granuloma model by injecting agar subcutaneously. Second, model mice were intragastricaly treated with different doses of water and alcohol extracts from for 3 and 7 days continually. Then the levels and activities of SOD, MDA, NO, NOS, GSH, GSH-Px of serum and hepatic tissue were detected after the last medication. Results The water extracted and alcohol extracted components could cause the level of MDA in serum and liver to increase, the activity of SOD corresponding declined, however the level of NO and NOS increased. In addition, the activity of GSH and GSH-Px declined. All the changes were aggravated in accordance with the enhancement of doses and time extension, and these parameters of all the medication administration groups had obvious difference with those of the blank control group. Conclusion The mechanism of the toxical and side effects on inflammatory mice caused by water and alcohol extract from may be related with the peroxidative damage mechanism.

Key words: different components, toxicity, liver damage mechanism, oxidative damage

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