Abstract
Purpose: To investigate the therapeutic effect of vitexin on neuropathic pain (NP) in a mouse model of chronic constriction injury (CCI).Methods: The CCI model was established by four chronic ligatures in the sciatic nerve. Vitexin was intraperitoneally administered (10 mg/kg, once daily) for 21 days. Mechanical withdrawal threshold (MWT) and paw withdrawal latency (PWL) were determined before and after the establishment of CCI model. The spinal cords were collected to measure mRNA levels by reverse-transcriptase polymerase chain reaction (RT-PCR) enzyme-linked immunosorbent assay (ELISA). Western blot was used to examine protein expression levels.Results: Vitexin reversed the CCI-induced reduction in MWT and PWL values, indicating that it lowered mechanical hypersensitivity response and hyperalgesia caused thermal stimulation (p < 0.05). The elevated levels of IL-6, IL-1β, and TNFα observed in CCI-treated mice were also inhibited by vitexin, suggesting that it suppressed pro-inflammatory cytokines. Moreover, vitexin attenuated CCI-induced activation of NF-κB signaling in CCI-treated mice (p < 0.05).Conclusion: Vitexin alleviates NP by inhibiting pro-inflammatory cytokines and NF-κB signaling in CCItreated mice. Thus, it is a potential target for NP treatment.
 Keywords: Vitexin, Neuropathic pain, Chronic constriction injury, Mechanical hypersensitivity, Hyperalgesia, NF-κB
Highlights
Pain result from a lesion or somatosensory nervous system dysfunction is called as neuropathic pain (NP) [1]
To investigate the therapeutic value of vitexin on NP, a constriction injury (CCI) mice model was established by four chronic ligatures in the sciatic nerve, Mechanical withdrawal threshold (MWT) value was measured
The mRNA expression and levels of IL-6, IL-1β, and TNFα were higher in the spinal cord from CCI mice than sham mice
Summary
Pain result from a lesion or somatosensory nervous system dysfunction is called as neuropathic pain (NP) [1]. The incidence of NP has remarkably increased, and about 15-25% of patients with chronic pain have NP [2]. Mice were grouped (n = 10/group): 1) sham, 2) CCI, and 3) CCI + Vitexin (Vit). CCI + Vit, mice after CCI surgery were intraperitoneally injected with vitexin (10 mg/kg, Tauto Biotechnology Co., Ltd., Shanghai, China) once daily for 21 days. CCI, mice after CCI surgery received normal saline as negative control. The NF-κB signaling pathway is closely related to multiple biological processes through regulating cytokine expression and immune responses [11]. The regulation of inflammatory cytokine gene expression caused by the activated NF-κB pathway have been proved to affect pain behavior [12]. Through inhibiting NF-κB signaling, dexmedetomidine relieved NP following chronic constriction injury (CCI) [13]. Considering the conclusion that vitexin could suppress the NF-κB pathway [14], it is hypothesized that vitexin may ameliorate NP by suppressing NF-κB activation
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