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<p>Paclitaxel-induced peripheral neuropathic pain (PIPNP) is a common and debilitating adverse effect of chemotherapy, with limited effective treatments. Electroacupuncture (EA) has demonstrated analgesic potential in various pain models, but its efficacy and mechanisms in PIPNP remain incompletely understood. This study aimed to evaluate the analgesic effect of EA in a murine model of PIPNP and investigate whether its mechanism involves modulation of the TLR4/P2X7-NLRP3 signaling pathway. A PIPNP model was established in male C57BL/6&#xa0;J mice by intraperitoneal injection of paclitaxel (cumulative dose 8&#xa0;mg/kg). Mice were randomly divided into control, PIPNP model, PIPNP with EA treatment at different intensities (0.5, 1.0, and 2.0&#xa0;mA), and sham EA groups. Mechanical allodynia and thermal hyperalgesia were assessed using von Frey filaments and hot plate tests, respectively. Immunofluorescence staining and western blotting were employed to analyze the expression of pain-related neurotransmitters (substance P, CGRP, p75) and key components of the TLR4/P2X7-NLRP3 signaling pathway in plantar tissues, dorsal root ganglia (DRG), and spinal cord. EA treatment, particularly at 1.0&#xa0;mA, significantly alleviated paclitaxel-induced mechanical allodynia and thermal hyperalgesia. Paclitaxel administration upregulated substance P, CGRP, and p75 in plantar tissues and activated the TLR4/P2X7-NLRP3 signaling pathway in DRG and spinal cord, as evidenced by increased expression of TLR4, P2X7, NLRP3, NF-κB, IL-1β, and IL-18. EA intervention markedly suppressed these changes, indicating its role in inhibiting neuroinflammation and modulating pain-related signaling. EA exerts analgesic effects in paclitaxel-induced neuropathic pain by attenuating the activation of the TLR4/P2X7-NLRP3 signaling pathway and reducing the expression of pain-related neurotransmitters.</p>

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The analgesic effect of electroacupuncture in alleviating paclitaxel-induced peripheral neuropathic pain and its possible mechanism relates to TLR4/P2X7-NLRP3 signaling pathway

  • 期刊论文

  • 发表日期：

    2026年5月12日

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  • Yuan-xi Zhou,
  • Man-ni Wang,
  • Juan-juan Xin,
  • Jing-wei Tan,
  • Xiao Sang,
  • Yu-xue Zhao

摘要

Paclitaxel-induced peripheral neuropathic pain (PIPNP) is a common and debilitating adverse effect of chemotherapy, with limited effective treatments. Electroacupuncture (EA) has demonstrated analgesic potential in various pain models, but its efficacy and mechanisms in PIPNP remain incompletely understood. This study aimed to evaluate the analgesic effect of EA in a murine model of PIPNP and investigate whether its mechanism involves modulation of the TLR4/P2X7-NLRP3 signaling pathway. A PIPNP model was established in male C57BL/6 J mice by intraperitoneal injection of paclitaxel (cumulative dose 8 mg/kg). Mice were randomly divided into control, PIPNP model, PIPNP with EA treatment at different intensities (0.5, 1.0, and 2.0 mA), and sham EA groups. Mechanical allodynia and thermal hyperalgesia were assessed using von Frey filaments and hot plate tests, respectively. Immunofluorescence staining and western blotting were employed to analyze the expression of pain-related neurotransmitters (substance P, CGRP, p75) and key components of the TLR4/P2X7-NLRP3 signaling pathway in plantar tissues, dorsal root ganglia (DRG), and spinal cord. EA treatment, particularly at 1.0 mA, significantly alleviated paclitaxel-induced mechanical allodynia and thermal hyperalgesia. Paclitaxel administration upregulated substance P, CGRP, and p75 in plantar tissues and activated the TLR4/P2X7-NLRP3 signaling pathway in DRG and spinal cord, as evidenced by increased expression of TLR4, P2X7, NLRP3, NF-κB, IL-1β, and IL-18. EA intervention markedly suppressed these changes, indicating its role in inhibiting neuroinflammation and modulating pain-related signaling. EA exerts analgesic effects in paclitaxel-induced neuropathic pain by attenuating the activation of the TLR4/P2X7-NLRP3 signaling pathway and reducing the expression of pain-related neurotransmitters.