Proanthocyanidins Inhibit the Transmission of Spinal Pain Information Through a Presynaptic Mechanism in a Mouse Inflammatory Pain Model.

Proanthocyanidins Inhibit the Transmission of Spinal Pain Information Through a Presynaptic Mechanism in a Mouse Inflammatory Pain Model.
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原花青素通过小鼠炎症性疼痛模型的突触前机制抑制脊髓疼痛信息的传递

DOI:
10.3389/fnins.2021.804722
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发表时间:
2021
影响因子:
4.3
通讯作者:
Chen T
Chen T
中科院分区:
医学2区
文献类型:
--
作者:
Fan H;Wu Z;Zhu D;Gu J;Xu M;Zhang M;Duan H;Li Y;Chen T

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炎性疼痛是临床疼痛中最常见的症状之一,严重影响患者的生活质量,但目前其治疗选择有限。原花青素是一组富含于植物和食物中的多酚类物质,据报道具有抗炎镇痛作用。然而,原花青素缓解中枢神经系统炎症性疼痛的机制尚不清楚。在本研究中,我们观察到鞘内注射原花青素抑制机械和热疼痛的敏感性在小鼠与完全弗氏佐剂(CFA)注射诱导的炎性疼痛。电生理结果进一步表明,原花青素抑制自发兴奋性突触后电流的频率,而不影响自发抑制性突触后电流或臂旁核投射神经元的内在特性。原花青素的作用可能是通过抑制背根神经节神经元中PI 3 K/Akt/mTOR通路分子的磷酸化激活来介导的。总之,鞘内注射原花青素通过抑制向脊髓上区发送伤害性信息的脊髓神经元的外周兴奋性输入,诱导小鼠明显的抗炎疼痛作用。
Inflammatory pain is one of the most common symptoms of clinical pain that seriously affects patient quality of life, but it currently has limited therapeutic options. Proanthocyanidins, a group of polyphenols enriched in plants and foods, have been reported to exert anti-inflammatory pain-alleviating effects. However, the mechanism by which proanthocyanidins relieve inflammatory pain in the central nervous system is unclear. In the present study, we observed that intrathecal injection of proanthocyanidins inhibited mechanical and thermal pain sensitivity in mice with inflammatory pain induced by Complete Freund’s Adjuvant (CFA) injection. Electrophysiological results further showed that proanthocyanidins inhibited the frequency of spontaneous excitatory postsynaptic currents without affecting the spontaneous inhibitory postsynaptic currents or the intrinsic properties of parabrachial nucleus-projecting neurons in the spinal cord. The effect of proanthocyanidins may be mediated by their inhibition of phosphorylated activation of the PI3K/Akt/mTOR pathway molecules in dorsal root ganglia neurons. In summary, intrathecal injection of procyanidin induces an obvious anti-inflammatory pain effect in mice by inhibiting peripheral excitatory inputs to spinal neurons that send nociceptive information to supraspinal areas.
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