电针对人重组肿瘤坏死因子诱导的气囊炎症模型大鼠环氧合酶基因和蛋白表达的影响

作者	单位
刘芳	浙江省中西医结合医院针灸科
方剑乔	浙江中医药大学第三临床医学院
邵晓梅	浙江中医药大学第三临床医学院
吴媛媛	浙江林学院

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中文摘要:

目的探讨电针对人重组肿瘤坏死因子(hrTNF)诱导的环氧合酶(COX)基因和蛋白表达的影响。方法 SPF级大鼠背部埋植一个经灭菌的聚四氟乙烯圆柱体建立气囊模型,10天后将确认无感染合格大鼠90只随机分为对照组、TNF模型组(简称模型组)、TNF电针组(简称电针组),每组30只,分别注射生理盐水和hrTNF造模,电针组即刻电针双侧曲池穴(2Hz,5mA,30min),分别于造模后1、5、24h抽取囊内液体,采用逆转录聚合酶链反应(RT-PCR)法及蛋白免疫印迹(Westernblot)法检测各组各时间点COX-2mRNA和蛋白表达。结果与对照组比较,模型组、电针组差异有统计学意义(P<0.05,P<0.01)),注射后24h电针组COX-2mRNA表达明显低于模型组(P<0.05),注射后1h电针组COX-2蛋白表达明显低于模型组(P<0.01)。结论电针能有效干预hrTNF-α诱导的COX-2mRNA和蛋白的表达;电针对COX-2的干预可能通过前炎症细胞因子调控途径。

英文摘要:

Objective To explore the intervention of electro-acupuncture(EA) on cycloxygenase(COX) mRNA and protein expression induced by human recombination tumor necrosis factor-α(hrTNF) .Methods Air sac model was established by implanted an autoclaved teflon chamber into back of rat(SPF grade) .Ten days after modeling,90 qualified rats,in them inflammation not detected,were randomly divided into three groups,the control group,the TNF model(model) group and the TNF + EA(TE) group,with 30 cases in each.To rats in the control group,1 mL of saline was injected into the sac,but to those in the model and TE groups,2 ng/mL hrTNF in a volume of 1 mL was used instead to induce local inflammatory responses.Immediately after then,EA(2 Hz,5 mA and persistent waves) was applied to bilateral Quchi points(LI11) of rats in the TE group for 30 min.Fluid in the sac was drawn out at various time points(1,5 and 24 h) after injection to measure the COX-2 mRNA expression by RT-PCR and COX-2 protein expression by Western blot.Results Level of COX-2 mRNA expression in the control group was significantly different to that in the other two groups(P <0.05 or P <0.01) .COX-2 mRNA expression at the 24th hour and COX-2 protein expression at the 1st hour were significantly lower in the TE group than those in the model group(P <0.05 and P <0.01) respectively.Conclusion EA could effectively intervene the mRNA and protein expression of COX-2 induced by hrTNF,which is possibly by way of pro-inflammatory cytokine regulating.

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