METHODS: This study established DNP model rats by intraperitoneally injecting a single high-dose streptozotocin; 2 Hz electroacupuncture was used to stimulate Zusanli (ST36) and Kunlun (BL60) of DNP rats daily from day 15 to day 21 after streptozotocin injection. Behavioral assay, quantitative PCR, immunofluorescence staining, and western blotting were used to study the analgesic mechanism of electroacupuncture.
RESULTS: The bradykinin B1 receptor (B1R) mRNA, nuclear factor-κB p65 (p65), substance P, and calcitonin gene-related peptide (CGRP) protein expression were significantly enhanced in SCDH of DNP rats. The paw withdrawal threshold was increased while body weight and fasting blood glucose did not change in DNP rats after the electroacupuncture treatment. The expression of B1R, p65, substance P, and CGRP in SCDH of DNP rats was also inhibited after the electroacupuncture treatment.
CONCLUSIONS: This work suggests that the potential mechanisms inducing the allodynia of DNP rats were possibly related to the increased expression of B1R, p65, substance P, and CGRP in SCDH. Downregulating B1R, p65, substance P, and CGRP expression levels in SCDH may achieve the analgesic effect of 2 Hz electroacupuncture treatment.
方法:本研究通过腹腔注射单一高剂量链脲佐菌素建立DNP大鼠模型;链脲佐菌素注射后第15天至第21天,每天用2Hz电针刺激DNP大鼠的足三里(ST36)和昆仑(BL60)。行为分析,定量PCR,免疫荧光染色,采用免疫印迹法研究电针的镇痛机制。
结果:缓激肽B1受体(B1R)mRNA,核因子-κBp65(p65),P物质,降钙素基因相关肽(CGRP)蛋白在DNP大鼠SCDH中表达显著增强。电针治疗后,DNP大鼠的爪缩阈值增加,而体重和空腹血糖没有变化。B1R的表达,p65,P物质,电针治疗后,DNP大鼠SCDH中的CGRP也受到抑制。
结论:这项工作表明,诱导DNP大鼠异常性疼痛的潜在机制可能与B1R的表达增加有关,p65,P物质,和CGRP在SCDH。下调B1R,p65,P物质,SCDH中CGRP的表达水平可能达到2Hz电针治疗的镇痛效果。