کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2741478 | 1148533 | 2013 | 6 صفحه PDF | دانلود رایگان |
Neuropathic pain is a pathological symptom experienced worldwide by patients suffering with nervous system dysfunction caused by various diseases. Treatment of neuropathic pain is always accompanied by a poor response and undesired adverse effects. Therefore, developing a novel “pain-kill” drug design strategy is critical in this field. Recent evidence demonstrates that neuroinflammation and immune response contributes to the development of neuropathic pain. Nerve damage can initiate inflammatory and immune responses, as evidenced by the upregulation of cytokines and chemokines. In this paper, we demonstrated that different chemokines and chemokine receptors (e.g., CX3CL1/CX3CR1, CCL2/CCR2, CCL3/CCR1, CCL4/CCR5 and CCL5/CCR5) serve as mediators for neuron–glia communication subsequently modulate nociceptive signal transmission. By extensively understanding the role of chemokines in neurons and glial cells in nociceptive signal transmission, a novel strategy for a target-specific drug design could be developed.
Journal: Acta Anaesthesiologica Taiwanica - Volume 51, Issue 3, September 2013, Pages 127–132