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原发性或继发性的骨癌往往伴有严重且棘手的疼痛问题。目前骨癌痛的发生机制尚不明确。本文研究首先证实,在接种MRMT-1肿瘤细胞的胫骨骨癌痛大鼠,背根神经节(DRG)P2X3受体表达和功能上调,并参与神经元兴奋性增加及骨癌痛。其次,神经元钙敏感蛋白(VILIP-1)氨基末端可与P2X3受体的C-末端直接作用,增加P2X3受体在细胞膜上的表达与功能。第三,在naive组大鼠的DRG神经元中,过表达VILIP-1增
Primary or secondary bone cancer is often accompanied by severe and intractable pain problems. The mechanism of bone cancer pain is not yet clear. This study first confirmed that expression and function of P2X3 receptor in dorsal root ganglion (DRG) were increased in the tibial bone cancer rats vaccinated with MRMT-1 tumor cells and involved in the increase of neuronal excitability and bone cancer pain. Second, the amino terminal of neuronal calcium-sensitive protein (VILIP-1) interacts directly with the C-terminal of P2X3 receptor to increase the expression and function of P2X3 receptor on the cell membrane. Third, over-expression of VILIP-1 was increased in naive group of DRG neurons