摘要
目的研究羟基红花黄色素A的镇痛作用及机制,为其研究开发提供理论依据。方法通过小鼠热板实验和醋酸诱发小鼠扭体反应实验研究羟基红花黄色素A的镇痛作用,采用Griess法和免疫印迹法研究小鼠免疫细胞RAW264.7中一氧化氮(NO)含量和MAPK/p38/iNOS信号通路的变化。结果羟基红花黄色素A(10、20 mg·kg^(-1))可以剂量依赖性的提高热板所致疼痛小鼠痛阈值(P <0.05),并可显著减少醋酸所致的小鼠扭体数(P <0.05)。细胞实验研究表明羟基红花黄色素A(0.1、1 mmol·L^(-1))可显著降低脂多糖(LPS)诱导的RAW264.7细胞的NO含量升高(P <0.05),并可以抑制RAW264.7细胞的MAPK/p38/iNOS信号通路的激活。结论羟基红花黄色素A具有一定的镇痛作用,其镇痛机制可能与抑制MAPK/p38/iNOS通路,继而减少NO的合成和释放有关。
Objective To explore the analgesic effect of safflomin A and its mechanism. Methods The analgesic effect of safflomin A was examined by the hot plate test and acetic acid-induced writhing response. The contents of NO and the activation of MAPK/p38/iNOS pathway in LPS-induced RAW264.3 were determined by Griess assay and Western blot. Results Safflomin A(10 and 20 mg·kg^-1) showed a significant prolongation of licking time in the hot plate test and the inhibition of acetic acid-induced writhing response in a dose-dependent manner(P< 0.05). Furthermore, the contents of NO and the activity of MAPK/p38/iNOS of RAW264.7 cells induced by LPS were inhibited by safflomin A(0.1 and 1 mmol·L^-1) treatment. Conclusion The analgesic of safflomin A is associated with suppressing the activation of MAPK/p38/iNOS pathway and subsequently reducing the synthesis and release of excessive NO.
作者
杨宇
史昌乾
佟杰
YANG Yu;SHI Chang-qian;TONG Jie(Liaoning Provincial Corps Hospital of Chinese People's Armed Police Forces,Shenyang 110034;Department of Pharmacy,Shenyang Red Cross Hospital,Shenyang 110034)
出处
《中南药学》
CAS
2019年第1期53-56,共4页
Central South Pharmacy
