The effect of emodin on complete Freund’s adjuvant (CFA)-induced inflammatory pain in rats and its potential molecular mechanism was investigated. For this, a rat model of inflammatory pain induced by CFA was established and rats were treated with emodin by intraperitoneal injection. The pain threshold was evaluated by the von Frey, thermo hyperalgesia, and cold plate tests. The mRNA expression of transient receptor potential channel ankyrin type-1 (Trpa1) and transient receptor potential vanilloid 1 (Trpv1) was detected by quantitative reverse transcription polymerase chain reaction, and the level of inflammatory cytokines was determined by enzyme-linked immunosorbent assay. The mechanical and thermal pain thresholds of CFA-treated rats were significantly lower than those of the control rats, while the paw withdrawal responses in response to cold stimulation were higher than that of the control group. Emodin treatment significantly improved CFA-induced hyperalgesia. Further results showed that emodin inhibits the upregulation of Trpa1 and Trpv1 mRNA expression in the dorsal root ganglion (DRG) of rats with inflammatory pain compared with the control group. Emodin also significantly reduced the levels of tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1β), and interleukin 6 (IL-6) in the serum of rats with inflammatory pain. Thus, emodin may inhibit hyperalgesia induced by inflammatory stimulation by downregulating the mRNA expression of Trpa1 and Trpv1 in DRG neurons and reducing the levels of TNF-α, IL-1β, and IL-6.

研究了大黄素对完全弗氏佐剂（CFA）诱导的大鼠炎症性疼痛的作用及其潜在的分子机制。为此，建立了由CFA诱导的炎性疼痛的大鼠模型，并通过腹膜内注射用大黄素治疗大鼠。通过von Frey，热痛觉过敏和冷板试验评估疼痛阈值。瞬时受体电位通道锚蛋白1型（Trpa1）和瞬时受体电位香草素1（Trpv1）的mRNA表达。通过定量逆转录聚合酶链反应检测），并通过酶联免疫吸附测定法测定炎性细胞因子的水平。CFA治疗组大鼠的机械和热痛阈值明显低于对照组，而冷刺激引起的爪缩缩反应高于对照组。大黄素治疗显着改善了CFA诱导的痛觉过敏。进一步的结果显示，抑制大黄素的上调TRPA1和TRPV1与对照组相比，炎性疼痛大鼠背根神经节（DRG）中的mRNA表达。大黄素还可以显着降低炎性疼痛大鼠血清中的肿瘤坏死因子α（TNF-α），白介素1β（IL-1β）和白介素6（IL-6）的水平。因此，可以大黄素通过下调的mRNA表达抑制由炎症刺激诱导的痛觉过敏TRPA1和TRPV1在DRG神经元和减少TNF-α，IL-1β和IL-6的水平。