川芎嗪对慢性肺源性心脏病患者趋化因子Fractalkine及肿瘤坏死因子-α表达的影响

作者	单位
李略	浙江省舟山人民医院呼吸内科
王良兴	浙江省温州医学院附属第一医院呼吸内科
董央庆	浙江省舟山人民医院呼吸内科
毛雨萍	浙江省舟山人民医院呼吸内科
陈志萍	浙江省舟山人民医院呼吸内科

摘要点击次数: 1299

全文下载次数: 533

中文摘要:

目的探讨趋化因子Fractalkine(FKN)、肿瘤坏死因子-α(TNF-α)与慢性肺源性心脏病(简称肺心病)的关系,揭示川芎嗪抑制肺动脉高压的作用机制。方法将35例确诊为慢性肺心病患者随机分为川芎嗪组(19例)及常规治疗组(16例),并选取18名健康体检者为健康组。常规治疗组给予常规治疗(哌拉西林/他唑巴坦针3.375 g静脉滴注,每天2次;左氧氟沙星针0.6 g静脉滴注,每天1次;氨溴索针60 mg静脉滴注,每天1次;多索茶碱针0.2 g静脉滴注,每天1次,均连用10～14天,并纠正酸碱失衡及电解质紊乱),川芎嗪组在常规治疗基础上加用盐酸川芎嗪(商品名:川青,每支120 mg,240 mg加入生理盐水注射液250 mL中静脉滴注,每天1次,连用10～14天),分别于治疗前后采用酶联免疫法检测血清FKN、TNF-α水平,应用多普勒超声仪检测治疗前后肺动脉压(mPAP)的变化。结果(1)治疗前常规治疗组、川芎嗪组血清FKN及TNF-α水平差异无统计学意义(P>0.05),但均高于健康组(均P<0.01);(2)川芎嗪组治疗后FKN、TNF-α及mPAP水平显著低于治疗前,且低于常规治疗组治疗后(P<0.05,P<0.01)。(3)FKN与TNF-α水平呈显著正相关(r=0.662,P<0.01)。结论(1)慢性肺心病患者存在FKN及TNF-α的高表达状态;(2)川芎嗪能抑制慢性肺心病患者FKN与TNF-α的表达,这可能是其降低肺动脉压的重要作用机制之一。

英文摘要:

Objective To reveal the relationship of chronic pulmonary heart disease(CPHD) with the chemotactic factor Fractalkine(FKN) and tumor necrosis factor-α(TNF-α),and to explore the action mechanism of tetramethylpyrazine(TMP) for suppressing pulmonary hypertension.Methods Patients with CPHD were randomly assigned to two groups,19 in Group A and 16 in Group B,and a control group(group C) consisting of 18 healthy adults was setup.Conventional treatment were given to all patients,which consisted of Piperacillin 3.375 g iv dripping twice a day,Levofloxacin 0.6 g + Ambroxol 60 mg + Doxofylline 0.2 g iv dripping once a day,all for 10-14 days,and acid-base and electrolytesim balance in patients were monitored and corrected.At the same time,TMP(trade name: Chuanqing,containing 120 mg of TMP in a 2 mL ampoule) was given additionally to patients in Group B at the dosage of 240 mg/d by adding in 250 mL of normal saline via iv dripping.Serum levels of FKN and TNF-α were detected before and after treatment by enzyme-linked immunoassay,and the change of mean pulmonary arterial pressure(mPAP) was measured as well.Results Before treatment,difference of FKN and TNF-α levels between the two patients′ groups were insignificant(P>0.05),but all higher than those in Group C respectively(P<0.01).While after treatment,the two indices and mPAP levels in Group B were statistically lower than those before treatment,also than those in Group A.Regression analysis showed a positive correlation between TNF-α and FKN(r=0.662,P<0.001).Conclusions A high blood FKN and TNF-α expression state exists in CPHD patients,which could be suppressed by TMP,and these suppressive effects may be one of the important mechanisms responsible for the pulmonary arterial pressure lowering action of TMP.

关闭