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目的:观察不同剂量雷公藤内酯醇(triptolide,TP)对佐剂性关节炎(adjuvant arthritis,AA)大鼠的镇痛作用,及其脊髓神经生物学机制。方法:SD大鼠50只,随机分成正常对照组、模型组及TP低、中、高剂量组。造模后14 d,TP各剂量组大鼠予相应剂量TP腹腔注射给药,1次/d,连续给药9 d。检测大鼠热痛阈,用免疫组织化学方法检测腰5(L5)脊髓背角和背根神经节(DRG)中NMDA受体Ⅱ型R1(NMDAR1)、西非单叶豆同工凝集素(BSIB4)结合位点表达变化情况。结果:治疗9 d后,模型组大鼠热痛阈显著低于正常对照组(P<0.01),TP各剂量组热痛阈显著高于模型组(P<0.05或P<0.01);免疫组化结果表明,模型组大鼠L5节段脊髓背角和DRG中NMD AR1、BSI-B4结合位点阳性表达水平显著升高(P<0.01),而TP各剂量组大鼠L5节段脊髓背角和DRG中NMDAR1、BSI-B4结合位点阳性表达水平低于模型组。结论:TP对AA大鼠具有良好镇痛作用,并能抑制AA大鼠脊髓背角和DRG中NMDAR1、BSI-B4结合位点的表达,这可能是TP镇痛作用机制之一。
OBJECTIVE: To observe the analgesic effect of different doses of triptolide (TP) on adjuvant arthritis (AA) in rats and its neurobiological mechanism of spinal cord. Methods: Fifty SD rats were randomly divided into normal control group, model group and TP low, medium and high dose groups. On the 14th day after modeling, rats in each dose group of TP were injected intraperitoneally with the corresponding dose of TP once a day for 9 days. The heat pain threshold was detected in rats. The expressions of NMDA receptor type II (NMDAR1), BSIB4 (BMSC) in the spinal dorsal horn and dorsal root ganglion (DRG) of lumbar 5 (L5) ) Binding site expression changes. Results: After 9 days of treatment, the heat pain threshold of the model group was significantly lower than that of the normal control group (P <0.01), and the heat pain threshold of each dose group was significantly higher than that of the model group (P <0.05 or P <0.01) The results showed that the positive expression of NMD AR1 and BSI-B4 in spinal dorsal horn and DRG in L5 segment of model rats were significantly increased (P <0.01), while the levels of L5 spinal cord The positive expression of NMDAR1 and BSI-B4 in DRG and DRG was lower than that in model group. CONCLUSION: TP has good analgesic effect on AA rats and inhibits the expression of NMDAR1 and BSI-B4 binding sites in spinal dorsal horn and DRG of AA rats, which may be one of the mechanisms of TP analgesia.