中国综合临床
中國綜閤臨床
중국종합림상
CLINICAL MEDICINE OF CHINA
2009年
5期
499-501
,共3页
哮喘%核因子-κB%单核细胞化学趋化蛋白-1
哮喘%覈因子-κB%單覈細胞化學趨化蛋白-1
효천%핵인자-κB%단핵세포화학추화단백-1
Asthma%NF-κB%Monecyte chemoactracttive peptide-1
目的 探讨核因子-κB(NF-κB)及单核细胞化学趋化蛋白-1(MCP-1)在支气管哮喘患者外周血中的表达,并观察用沙美特罗替卡松、布地奈德加沙丁胺醇治疗时其的影响.方法 81例哮喘患者随机分为沙美特罗替卡松组(41例)和布地奈德加沙丁胺醇组(40例),另以健康人45例为对照组;用ELISA法测定各组外周血单个核细胞(PBMC)中NF-κB活性和MCP-1水平.结果 ①沙美特罗替卡松治疗组PBMC中NF-κB活性[(1.32±0.36)ng/L]及MCP-1水平[(66.89±5.62)ng/L]和布地奈德加沙丁胺醇治疗组PB-MC中NF-κB活性[(1.70±0.39)ng/L]及MCP-1水平[(73.35±7.52)ng/L]明显高于正常对照组[(0.89±0.34)ng/L及(58.63±8.24)ng/L,P均<0.001];②沙美特罗替卡松治疗组PBMC中NF-κB活性和MCP-1水平明显低于布地奈德加沙丁胺醇治疗组(P均<0.001).结论 NF-κB基因及其调控蛋白MCP-1参与了哮喘的发病过程,激素和β2受体激动刺联用治疗后可延缓哮喘的发病.
目的 探討覈因子-κB(NF-κB)及單覈細胞化學趨化蛋白-1(MCP-1)在支氣管哮喘患者外週血中的錶達,併觀察用沙美特囉替卡鬆、佈地奈德加沙丁胺醇治療時其的影響.方法 81例哮喘患者隨機分為沙美特囉替卡鬆組(41例)和佈地奈德加沙丁胺醇組(40例),另以健康人45例為對照組;用ELISA法測定各組外週血單箇覈細胞(PBMC)中NF-κB活性和MCP-1水平.結果 ①沙美特囉替卡鬆治療組PBMC中NF-κB活性[(1.32±0.36)ng/L]及MCP-1水平[(66.89±5.62)ng/L]和佈地奈德加沙丁胺醇治療組PB-MC中NF-κB活性[(1.70±0.39)ng/L]及MCP-1水平[(73.35±7.52)ng/L]明顯高于正常對照組[(0.89±0.34)ng/L及(58.63±8.24)ng/L,P均<0.001];②沙美特囉替卡鬆治療組PBMC中NF-κB活性和MCP-1水平明顯低于佈地奈德加沙丁胺醇治療組(P均<0.001).結論 NF-κB基因及其調控蛋白MCP-1參與瞭哮喘的髮病過程,激素和β2受體激動刺聯用治療後可延緩哮喘的髮病.
목적 탐토핵인자-κB(NF-κB)급단핵세포화학추화단백-1(MCP-1)재지기관효천환자외주혈중적표체,병관찰용사미특라체잡송、포지내덕가사정알순치료시기적영향.방법 81례효천환자수궤분위사미특라체잡송조(41례)화포지내덕가사정알순조(40례),령이건강인45례위대조조;용ELISA법측정각조외주혈단개핵세포(PBMC)중NF-κB활성화MCP-1수평.결과 ①사미특라체잡송치료조PBMC중NF-κB활성[(1.32±0.36)ng/L]급MCP-1수평[(66.89±5.62)ng/L]화포지내덕가사정알순치료조PB-MC중NF-κB활성[(1.70±0.39)ng/L]급MCP-1수평[(73.35±7.52)ng/L]명현고우정상대조조[(0.89±0.34)ng/L급(58.63±8.24)ng/L,P균<0.001];②사미특라체잡송치료조PBMC중NF-κB활성화MCP-1수평명현저우포지내덕가사정알순치료조(P균<0.001).결론 NF-κB기인급기조공단백MCP-1삼여료효천적발병과정,격소화β2수체격동자련용치료후가연완효천적발병.
Objective To explore the expression of the nuclear factor -κB (NF-κB) regulating monocyte ehemoactracttive peptide -1 ( MCP-1) in asthma patients, and investigate the effect of seretide, budesonide and vento-lin. Methods 81 asthma patients were randomly divided into seretide therapy group and budesonide and ventolin therapy group. The NF-κB activation in PBMC and the plasma concentrations of MCP-1 were measured by ELISA. ventolin therapy group (1.70±0.39) ng/L of asthma patients were significantly higher than that control group (0.89±0.34) ng/L ( P<0.001 ) ; The plasma MCP-1 level in seretide therapy group ( 66.89±5.62 ) ng/L and in budesonide and ventolin therapy group (73.35±7.52 ) ng/L of asthma patients were also significantly higher than level of seretide therapy group in asthma patients were significantly lower than budesonide and ventolin therapy group (P <0.001 ). Conclusion NF-κB gene and its regulating protein MCP-1 may be involved in asthma. Glucocotios-teroid and beta2 agonists combination may prolong the process of asthma.
