【摘 要】
：
Objective: To observe the P2Y1 receptor, PLC-β, IP3 receptor and intracellular [Ca2+]i of dorsal root ganglia (DRG) neurons by using electroacupuncture at Tianshu (ST25) and Shangjuxu (ST37) in irrita
【机 构】
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Shanghai Research Institute of Acupuncture and Meridian, Shanghai University of Traditional Chinese
【出 处】
：
2014第五届国际神经科技大会暨2014首届国际高科技针灸和中西医结合大会
论文部分内容阅读
Objective: To observe the P2Y1 receptor, PLC-β, IP3 receptor and intracellular [Ca2+]i of dorsal root ganglia (DRG) neurons by using electroacupuncture at Tianshu (ST25) and Shangjuxu (ST37) in irritable bowel syndrome (IBS) rats with visceral hypersensitivity.Method: IBS visceral hypersensitivity model rats were made by colorectal distention stimulation of balloons, Rats were randomly divided into three groups including normal group (N group), model group (M group) and electroacupuncture group (EA group).EA group was treated by electroacupuncture at ST25 and ST37.After treatment, the expressions of P2Y 1 receptor, PLC-β and IP3 receptor were detected by irnmunohistochemical methods.Intracellular [Ca2+]i concentration of DRG neurons was detected by laser scanning confocal microscope technique after DRG neurons culture.Results: IBS visceral hypersensitivity model was established successfully.Body weight of rats in M group was significantly decreased compared with N group (P< 0.01), and was increased in EA compared with M group (P< 0.01).The AWR scores, expressions of P2Y1 receptor, PLC-β and IP3 receptor, intracellular [Ca2+]i concentration of DRG neurons in M group were significantly increased compared with N group (P< 0.01), and were decreased in EA compared with M group (P< 0.01).Conclusions: EA has pronounced effects on IBS rats with visceral hypersensitivity.High expressions of P2Y1 receptor, PLC-β and IP3 receptors in visceral hypersensitivity rats can be down regulated by EA effectively, also, increased intracellular [Ca2+]i concentration caused by P2Y1 receptor signal transduction pathways of DRG neurons can be inhibited by EA too.This may be one of the mechanisms of EA in treating visceral hypersensitivity.
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