有氧运动缓解肥胖大鼠背根神经节持续受压后神经病理性疼痛的机制研究

Obese patients are more prone to hyperalgesia and more difficult to treat. Aerobic exercise is an effective way to reduce fat, lose weight, and can relieve neuropathic pain. But the mechanism remains unclear. Orphan G protein coupled receptor GRP40 which involved in lipid metabolism and mechanism of neuropathic pain can regulate cell metabolism, proliferation and apoptosis through MAPK signaling pathway, apoptosis and pain related neurons. Therefore we assume that the GRP40-MAPK pathway regulates neuronal apoptosis and decrease neuropathic pain on obese rat with dorsal root ganglion chronic compression(CCD) after aerobic exercise. Obese CCD rats model is established and giving aerobic exercise training. The biochemical indexes of lipid metabolism in rats, the mechanical allodynia and thermal hyperalgesia changes are detected. We also detect the expression of GRP40, MAPK and neuron apoptosis in dorsal root ganglion and spinal dorsal horn. The subject of this study is in order to investigate the mechanism of GPR40-MAPK pathway in regulation of neuronal apoptosis in the aerobic exercise related pain relief in obese CCD rats.

肥胖患者更易产生痛觉过敏，且治疗难度更大。有氧运动是减脂、减重的有效方法，并可缓解神经病理性疼痛，其机制不明。G蛋白偶联受体(GPCRs)中的孤儿受体GRP40参与脂代谢及神经病理性疼痛机制，GPCRs可通过MAPK信号通路调节细胞代谢、增殖与凋亡，神经元的凋亡与疼痛密切相关。因此我们设想GRP40-MAPK通路调控神经元的凋亡而介导有氧运动对肥胖大鼠背根神经节持续受压后（CCD）神经病理性疼痛的缓解。我们拟建立肥胖大鼠CCD模型，对大鼠进行饮食控制及有氧运动训练，检测大鼠脂代谢相关生化指标变化；观察大鼠机械痛敏及热痛敏变化；检测背根神经节及脊髓背角GRP40、MAPK及神经元凋亡。以期明确GPR40-MAPK通路调控的神经元凋亡在有氧运动缓解肥胖大鼠神经病理性疼痛中的调控机制。