Eriocalyxin B inhibits inflammation induced by CCI-induced microglia activation to relieve neuropathic pain through inhibition of JAK2/STAT3 and NF-κB pathways

Zhifeng Sheng, Xiao-qing Pan
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Abstract

Neuropathic pain is a very troublesome disease that seriously affects human life. Eriocalyxin B (EriB) has been revealed to attenuate various diseases through its anti-inflammatory effects, but its regulatory effects on neuro-pathic pain remains unclear. The paw withdrawal threshold and paw withdrawal thermal latency were detected through mechanical allodynia and thermal hyperalgesia tests. The spinal injury was assessed through hematoxylin and eosin staining. The cell apoptosis was measured through terminal deoxynucleotide transferase-mediated dUTP nick end-labeling assay. The protein expressions were examined through Western blot analysis. The mRNA expression was examined through reverse transcription-quantitative polymerase chain reaction. The ionized calcium-binding adaptor molecule 1 level in the spinal cord was evaluated through immunofluorescence assay. The levels of tumor necrosis factor-α, interleukin (IL)-1β, and IL-6 were measured through enzyme-linked-immunosorbent serologic assay. The chronic constriction injury (CCI) rat model was constructed for the study. Our results demonstrated that EriB relieved CCI-stimulated neuropathic pain and nerve damage. In addition, the enhanced neural apoptosis mediated by CCI induction was reduced after EriB treatment. In addition, EriB inhib-ited CCI-induced microglia activity and inflammation. At last, the Janus kinase 2–signal transducer and activator of transcription 3 (JAK2/STAT3) and nuclear factor kappa B (NF-κB) pathways were activated in CCI rat model, which were attenuated following EriB treatment. Importantly, EriB (10 mg/kg) had a strong effect that was similar to the positive control (1-μg/kg dexmedetomidine), suggesting that EriB may be an effective drug for neuropathic pain. This study demonstrated that EriB inhibited inflammation caused by CCI-induced microglia activation to relieve neuropathic pain through inhibition of JAK2/STAT3 and NF-κB pathways. This study may highlight the regulatory functions of EriB in the treatment of neuropathic pain.
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Eriocalyxin B通过抑制JAK2/STAT3和NF-κB通路,抑制cci诱导的小胶质细胞激活引起的炎症,减轻神经性疼痛
神经性疼痛是一种非常麻烦的疾病,严重影响人类的生活。Eriocalyxin B (EriB)已被发现通过其抗炎作用减轻多种疾病,但其对神经性疼痛的调节作用尚不清楚。通过机械异常性痛和热痛觉过敏试验检测足部戒断阈值和足部戒断热潜伏期。苏木精和伊红染色评估脊髓损伤。通过末端脱氧核苷酸转移酶介导的dUTP缺口末端标记法检测细胞凋亡。Western blot检测蛋白表达。逆转录-定量聚合酶链反应检测mRNA表达。采用免疫荧光法测定脊髓内钙结合受体分子1的水平。采用酶联免疫吸附血清学法检测肿瘤坏死因子-α、白细胞介素(IL)-1β、IL-6水平。建立慢性缩窄性损伤大鼠模型。我们的研究结果表明,EriB减轻了cci刺激的神经性疼痛和神经损伤。此外,经EriB处理后,CCI诱导的神经细胞凋亡增强有所减弱。此外,EriB抑制cci诱导的小胶质细胞活性和炎症。最后,在CCI大鼠模型中,Janus kinase 2-signal transducer and activator of transcription 3 (JAK2/STAT3)和nuclear factor kappa B (NF-κB)通路被激活,EriB处理后这些通路被减弱。重要的是,EriB (10 mg/kg)具有与阳性对照(1-μg/kg右美托咪定)相似的强效,表明EriB可能是一种治疗神经性疼痛的有效药物。本研究表明,EriB通过抑制JAK2/STAT3和NF-κB通路,抑制cci诱导的小胶质细胞激活引起的炎症,从而缓解神经性疼痛。本研究可能进一步揭示EriB在神经性疼痛治疗中的调控作用。
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