邱氏穴对肾绞痛大鼠模型肾组织 PGI2、TXA2 和 5-HT 表达的影响

Effect of Qiu'spointon expressions of PGI2,TXA2 and 5-HT inratm odelofrenalcolic

摘要:

观察邱氏穴对肾绞痛大鼠模型中肾组织中前列环素（PGI2）、血栓素 A2（TXA2）以及 5 羟色胺（5-HT）表达的影响。方法 将 SD 大鼠分为 3 组：正常组、模型组和邱氏穴组。模型组与邱氏穴组采用 1%乙二醇和 1%氯化铵水溶液作为诱石剂自由饮水 10 d 建立草酸钙结石致大鼠肾绞痛模型，邱氏穴组采用龙虎交战复合手法针刺大鼠邱氏穴，通过观察大鼠行为学和肾组织病理切片变化，检测肾组织中 PGI2、TXA2 和5-HT 表达来判定邱氏穴对肾绞痛的影响作用。结果 正常组与邱氏穴组中痛阈值测定及自发性疼痛评分均较模型组降低（ <0.05），模型组中 PGI2、TXA2 和 5-HT 表达均较正常组及邱氏穴组升高（ <0.05），正常组与邱氏穴组 PGI2、TXA2 和 5-HT 表达比较差异无统计学意义（ >0.05），邱氏穴组中 PGI2/TXA2 比值与正常组比较差异有统计学意义（ <0.05），与模型组中差异无统计学意义（ >0.05）。结论 邱氏穴复合针刺手法对肾绞痛大鼠模型具有镇痛作用，推测其作用机制为通过抑制炎症介质 PGI2、TXA2 及神经递质 5-HT 合成，减轻 5-HT 致痛作用。

Abstract:

ToobservetheeffectofQiu'spointon theexpressionsofPGI2,TXA2 and 5-HT in therats with renalcolic.M ethods The SD rats were randomly divided into three groups:normalgroup,modelgroup and Qiu'spointgroup.In themodeland Qiu'spointgroups,1% ethyleneglycoland1% ammonium chloridewereusedas lurestoneagentstoestablish therenalcolicmodelinduced bycalcium oxalatestonein 10 days.Theratsin theQiu's pointgroupweregivenacupunctureon Qiu'spointwith dragon-tigerfightingneedlingmethod.Then thebehaviorand pathologicalchangesofkidneytissueswereobserved in thethreegroups,and theexpressionsofTXA2,PGI2 and 5-HT in the renaltissues were detected.Results The pain threshold value,the spontaneous pain score and the expressionsofTXA2,PGI2 and 5-HT ofthenormaland Qiu'spointgroupsweresignificantlylowerthan those of the modelgroup( < 0.05);however,therewasnosignificantdifferencein theTXA2,PGI2 or5-HT expression between thenormalgroup and theQiu'spointgroup( > 0.05).ThePGI2/TXA2 ratio wassignificantly differentbetween the Qiu'spointgroup and thenormalgroup ( < 0.05),butnotsignificantly differentbetween the Qiu'spointgroup and the model group ( > 0.05). Conclusions Dragon-tiger fighting needling method on Qiu's point can achieve analgesic effect in the treatment with renal colic rats, the mechanism is perhaps inhibiting the synthesis of inflammatorymediatorsTXA2 and PGI2 and neurotransmitter5-HT,and relievingthepain induced by5-HT.