慢性神经病理性痛大鼠背根神经节P2Y2受体mRNA的表达

P2Y2 receptor mRNA expression in dorsal root ganglion in a rat model of chronic neuropathic pain

目的评价背根神经节（DRG）P2Y2受体mRNA的表达在大鼠慢性神经病理性痛中的作用。方法SPF级大鼠24只,体重150～200g,雌雄不拘,随机分为2组：假手术组（S组）和慢性神经痛组（N组）,每组12只。N组结扎左侧坐骨神经建立大鼠慢性压迫性损伤（CCI）模型,S组只暴露,不结扎左侧坐骨神经。2组分别于CCI前1d、CCI后1、4、7、10、14 d进行行为学观察,测定大鼠双后肢热痛阈和机械痛阈,并分别于CCI后7、14 d各取6只大鼠断颈处死,取双侧L（4-6）背根神经节,RT-PCR法测定P2Y2受体mRNA的表达。结果两组CCI后4 d热痛阈、机械痛阈明显降低（P〈0.05）,持续至CCI后14 d;N组左侧DRG P2Y2受体mRNA表达较右侧明显下调,CCI后14 d较CCI后7 d下调（P〈0.05）;与S组右侧比较,N组DRG P2Y2受体mRNA表达差异无统计学意义（P〉0.05）。结论背根神经节P2Y2受体mRNA的表达下调参与了大鼠慢性神经病理性痛的形成。

Objective To investigate the changes in P2Y2 receptor mRNA expression in lumbar dorsal root ganglion neurous induced by chronic constriction injury （ CCI）. Methods Twenty-four SD rats of both sexes weighing 150-200 g were randomly divided into 2 groups （ n = 12 each） ： group A sham operation （S） and group B CCI. The animals were anesthetized with intraperitoneal 10% chloral hydrate 0.3 g/kg. Neuropathic pain was induced by chronic constrictive injury. The left sciatic nerve was exposed and 4 ligatures were placed on the sciatic nerve at 1 mm intervals with 4-0 silk thread. In sham operation group the left sciatic nerve was exposed but not ligated. Pain threshold to noxious thermal stimuli and mechanical stimulation with yon Frey filaments was measured for both hindlimbs before （baseline） and at days 1, 4, 7, 10 and 14 after operation and compared. Six animals each were killed on day 7 and 14 in each group. Bilateral L4-6 dorsal root ganglions were removed and crushed and total RNA was extracted and the expression of P2Y2 receptor mRNA was determined by RT-PCR. Results Thermal hyperalgesia and tactile allodynia were detected 4 days after operation and reached the peak on the 14th day. P2Y2 receptor mRNA expression in homolateral lumbar DRGs was down-regulated as compared with that in contralateral DRGs in CCI group. There was no significant difference in P2Y2 receptor mRNA expression in DRGs between the two sides in sham operation group. Conclusion Down-regulation of P2Y2 receptor gene expression in DRGs is involved in the mechanism of chronic neuropathic pain.