赵晶晶, 武文星, 朱昭颖, 刘睿, 宿树兰, 郭盛, 段金廒. 牦牛角对LPS诱导发热大鼠模型的解热活性评价及机制研究[J]. 南京中医药大学学报, 2022, 38(10): 936-944. DOI: 10.14148/j.issn.1672-0482.2022.0936
引用本文: 赵晶晶, 武文星, 朱昭颖, 刘睿, 宿树兰, 郭盛, 段金廒. 牦牛角对LPS诱导发热大鼠模型的解热活性评价及机制研究[J]. 南京中医药大学学报, 2022, 38(10): 936-944. DOI: 10.14148/j.issn.1672-0482.2022.0936
ZHAO Jing-jing, WU Wen-xing, ZHU Zhao-ying, LIU Rui, SU Shu-lan, GUO Sheng, DUAN Jin-ao. Evaluation of Antipyretic Activity and Potential Mechanism of Yak Horn on LPS-Induced Fever Rat Model[J]. Journal of Nanjing University of traditional Chinese Medicine, 2022, 38(10): 936-944. DOI: 10.14148/j.issn.1672-0482.2022.0936
Citation: ZHAO Jing-jing, WU Wen-xing, ZHU Zhao-ying, LIU Rui, SU Shu-lan, GUO Sheng, DUAN Jin-ao. Evaluation of Antipyretic Activity and Potential Mechanism of Yak Horn on LPS-Induced Fever Rat Model[J]. Journal of Nanjing University of traditional Chinese Medicine, 2022, 38(10): 936-944. DOI: 10.14148/j.issn.1672-0482.2022.0936

牦牛角对LPS诱导发热大鼠模型的解热活性评价及机制研究

Evaluation of Antipyretic Activity and Potential Mechanism of Yak Horn on LPS-Induced Fever Rat Model

  • 摘要:
      目的  基于脂多糖(LPS)诱导发热大鼠模型评价牦牛角解热活性并探讨其作用机制, 以期为牦牛角新资源药材与开发利用提供科学依据。
      方法  以大鼠肛温变化值及体温反应指数评价牦牛角解热活性; 采用ELISA试剂盒测定下丘脑中PGE2、cAMP的含量及血清中TNF-α与IL-1β的含量, 并结合超高压液相色谱飞行时间质谱法(UHPLC-Q-TOF-MS)检测发热大鼠血浆中内源性标志物, 探索牦牛角解热机制。
      结果  牦牛角给药后1、2、3 h大鼠体温明显下降(P < 0.05), 低剂量组TNF-α及cAMP水平均显著降低(P < 0.01), 高剂量组cAMP水平显著降低(P < 0.01), 牦牛角给药组均能抑制IL-1β与PGE2水平。从空白组与模型组血浆样本中共鉴定出15个潜在差异代谢物, 牦牛角高剂量给药后可显著回调其中11个代谢物, 主要包括磷脂酰乙醇胺、鞘磷脂、腺嘌呤、琥珀酸、L-苏氨酸、4-羟脯氨酸、磷脂酰胆碱、溶血性磷脂酰乙醇胺等, 主要涉及甘油磷脂代谢通路。
      结论  牦牛角解热活性确切, 其作用机制可能与抑制内源性致热源与中枢体温正性调节介质释放、调节脂质代谢密切相关。

     

    Abstract:
      OBJECTIVE  To evaluate the antipyretic activity of yak horn and explore its mechanism based on LPS-induced fever rat model, so as to provide scientific basis for new resources of yak horn medicinal materials.
      METHODS  Based on LPS-induced fever rat model, the antipyretic activity of yak horn was evaluated by anal temperature change value and body temperature response index of rats. The levels of PGE2 and cAMP in hypothalamus and TNF-α and IL-1β in serum were determined by ELISA kits. Combined with the detection of endogenous markers in plasma of rats with fever by UHPLC-Q-TOF-MS, the antipyretic mechanism of yak horn was explored.
      RESULTS  The body temperature of rats significantly decreased at the 1st, 2nd and 3rd hour after yak horn powder was delivered (P < 0.05), the levels of TNF-α and cAMP in the low dose yak horn group significantly decreased (P < 0.01), and the level of cAMP in the high dose yak horn group significantly decreased (P < 0.01). The expression of IL-1β and PGE2 was inhibited in the yak horn powder administration groups. 15 potential differential metabolites in plasma samples between blank group and model group were identified, while high dose yak horn significantly regulated 11 metabolites, including phosphatidyl ethanolamine, sphingomyelin, adenine, succinic acid, L-alanine, 4-hydroxyproline, phosphatidyl choline, hemolytic, phosphatidyl ethanolamine and so on, mainly involving glycerol phospholipid metabolism pathways.
      CONCLUSION  Yak horn shows definitely antipyretic activity, and its mechanism may be related to the inhibition of endogenous heat source, the release of positive regulatory medium of central body temperature, and the regulation of lipid metabolism.

     

/

返回文章
返回