神经病理性疼痛发生机制的研究进展(3)
慢性疼痛是最常见的神经病理性疼痛的表现,极大地影响患者的生活质量,因此,对神经病理性疼痛的发生、发展与维持机制进行研究,可有针对性地缓解疼痛,更有效地控制疼痛,故有大量神经病理性疼痛动物实验模型的建立,其主要目的为寻找疼痛发生机制。星形胶质细胞抑制剂氟代枸橼酸可降低星形胶质细胞在发生神经病理性疼痛后的表达水平从而达到镇痛目的;氯胺酮可通过抑制星形胶质细胞的活化从而达到镇痛目的。低浓度河豚毒素(TTX)可抑制糖尿病动物C-纤维的机械痛敏[25]。鞘内注射TNF-α抑制剂可以缓解相应类型的疼痛。从基因表达方面入手,通过敲除P2X4受体、TNFR1、TNFR2基因,使其不能转录、翻译、在体内合成相应蛋白质,阻断疼痛信号传导,或是干扰其在者体内的过度表达,以起到缓解疼痛目的的作用。目前已明确的研究成果中通过基因、细胞信息传导、受体介导导致神经病理性疼痛的研究略显不够。需要积极地探索并研究相关机制,以寻找临床更有效的治疗方法。
[参考文献]
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[7] Carrison CJ,Dougherty PM,Kajarkler KC,et al.Staining of glial fibrillary acidic protein (GFAP) in lumber spinal cord increases following a sciatic nerve constriction injury[J].Brain Res,1991,565(1):1-7.
[8] Zhang H,Yoon SY,Zhang H,et al.Evidence that spinal astrocytes but not microglia contribute to the pathogenesis of Paclitaxel-induced painful neuropathy[J].J Pain,2012:13(3):293-303.
[9] Liu T,Gao YJ,Ji RR.Emerging role of Toll-like receptors in the control of pain and itch[J].Neurosci Bull,2012,28(2):131-144.
[10] Siniscalco D,Giordano C,Risso F,et al.Role of neurotrophins in neuropathic pain[J].Current Neuropharmacology,2011,9(4):523-529.
[11] Cao Y,Wang H,Chiang CY,et al.Pregabalin suppresses nociceptive behavior and central sensitization in a rat trigeminal neuropathic pain model[J]. J Pain,2013,14(2):193-204.
[12] Kuner R.Central mechanisms of pathological pain[J].Nat Med,2010, 16(11):1258-1266.
[13] Peters CM,Ghilari JR,Keyser CP,et al.Tumor-induced in jury of primary afferent sensory nerve fibers in bone cancer pain[J].Exp Neurol,2005,193(1):85-100.
[14] Hulse R,Wynick D,Donaldson LF.Intact cutaneous C fiber afferent properties in mechanical and cold neuropathic allodynia[J].Eur J Pain,2010,14(6):565. (范顺意 李亦梅)
[参考文献]
[1] Haan M,Attal N,Backonja M,et al.NeuPSIG guidelines on neuropathic pain assessment[J].Pain,2011,152(1):14-27.
[2] Pizzo PA,Clark NM.Alleviating suffering 101—pain relief in the United States[J].N Engl J Med,2012,366(3):197-199.
[3] Abougalambou SS,Abougalambou AS.Explorative study on diabetes neuropathy among type Ⅱdiabetic patients in Universiti Sains Malaysia Hospital[J].Diabetes Metab Syndr,2012,6(3):167-172.
[4] Singh R,Kishore N,Kaur N.Diabetic peripheral neuropathy:current perspective and future directions[J].Pharmacol Res,2014,80:21-35.
[5] Cheng CF,Cheng JK,Chen CY,et al.Mirror-image pain is mediated by nerve growth factor produced from tumor necrosis factor alpha-activated satellite glia after peripheral nerve injury[J].Pain,2014,155(5):906-920.
[6] 邵林华,陈亦华,郑龙,等.颅脑损伤患者血清GFAP含量变化及其临床意义[J].全科医学临床与教育,2011,9(3):255-257.
[7] Carrison CJ,Dougherty PM,Kajarkler KC,et al.Staining of glial fibrillary acidic protein (GFAP) in lumber spinal cord increases following a sciatic nerve constriction injury[J].Brain Res,1991,565(1):1-7.
[8] Zhang H,Yoon SY,Zhang H,et al.Evidence that spinal astrocytes but not microglia contribute to the pathogenesis of Paclitaxel-induced painful neuropathy[J].J Pain,2012:13(3):293-303.
[9] Liu T,Gao YJ,Ji RR.Emerging role of Toll-like receptors in the control of pain and itch[J].Neurosci Bull,2012,28(2):131-144.
[10] Siniscalco D,Giordano C,Risso F,et al.Role of neurotrophins in neuropathic pain[J].Current Neuropharmacology,2011,9(4):523-529.
[11] Cao Y,Wang H,Chiang CY,et al.Pregabalin suppresses nociceptive behavior and central sensitization in a rat trigeminal neuropathic pain model[J]. J Pain,2013,14(2):193-204.
[12] Kuner R.Central mechanisms of pathological pain[J].Nat Med,2010, 16(11):1258-1266.
[13] Peters CM,Ghilari JR,Keyser CP,et al.Tumor-induced in jury of primary afferent sensory nerve fibers in bone cancer pain[J].Exp Neurol,2005,193(1):85-100.
[14] Hulse R,Wynick D,Donaldson LF.Intact cutaneous C fiber afferent properties in mechanical and cold neuropathic allodynia[J].Eur J Pain,2010,14(6):565. (范顺意 李亦梅)