缓激肽B1受体与疼痛

Bradykinin B1 receptors(B1R) and pain

缓激肽B1受体(bradykinin 1 receptors,B1Rs)是与Gq蛋白相偶联的受体。正常状态下,B1R除了在神经系统中(如脊髓背角浅层和感觉神经节)有少数表达外,其他机体组织中几乎不存在。在炎症或者神经受损的情况下,脊髓背角浅层和感觉神经节B1R表达量大大上升,参与炎性疼痛和神经病理性疼痛的产生和维持。近年来的研究表明,B1R在糖尿病性神经病理疼痛的发病中起着重要的作用。阻断B1R能有效抑制糖尿病诱发的热痛觉过敏和冷觉及触觉超敏。此外,B1R和癌症痛的发生也有密切关系,所以,对B1R的研究可能会为治疗这些临床顽症提供新的靶点。

Abstract： Bradykinin 1 receptors （B1Rs） are coupled with Gq protein. In the normal condition, B1Rs are not expressed in the tissues except in the nervous system, such as superficial laminae of spinal dorsal horn and sensory ganglion. The expression of B1R in the spinal cord and DRG is greatly upregulated following inflammation and nerve injury, contributing to the induction and maintainence of inflammatory and neuropathic pain. Recently, studies have demonstrated that B1Rs play a pivotal role in diabetic neuropathic pain. Blockade of B1Rs can inhibit diabetes-induced heat hyperalgesia as well as cold and mechanical allodynia. In addition, B 1 Rs are also involved in cancer pain, so studies of B 1 Rs may provide a novel target for the treatment. Key words： bradykinin B 1 receptor; inflammatory pain; neuropathic pain