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

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 hematox-ylin and eosin staining. The cell apoptosis was measured through terminal deoxynucleotide transferase-medi-ated 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 ion-ized calcium-binding adaptor molecule 1 level in the spinal cord was evaluated through immunofluorescence assay. The levels of tumor necrosis factor-alpha, interleukin (IL)-1 beta, 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-kappa B) 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-mu g/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-kappa B pathways. This study may highlight the regulatory functions of EriB in the treatment of neuropathic pain.