Objective To explore the relationship between heat-shock protein 70-2 gene +1267A/G polymorphism(HSP70-2 gene +1267A/G polymorphism) and serum level of high sensitivity C-reactive protein(Hs-CRP) in patients with coro...Objective To explore the relationship between heat-shock protein 70-2 gene +1267A/G polymorphism(HSP70-2 gene +1267A/G polymorphism) and serum level of high sensitivity C-reactive protein(Hs-CRP) in patients with coronary artery disease(CAD).Methods Serum Hs-CRP level and HSP70-2 gene +1267A/G polymorphism were detected in 185 patients with CAD.HSP70-2 gene +1267A/G polymorphism was screened by polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP).Results The genotype distribution of the HSP70-2 gene +1267A/G polymorphism was as follows: AA was in 24 of 185 patients(12.97%),AG in 93 of 185 patients(50.27%) and GG in 68 of 185 patients(36.76%).Patients with GG、AG subtype had higher Hs-CRP levels compared with carriers of the AA subtype(4.5±1.8mg/L,3.2±1.2mg/L and 2.7±1.1mg/L,respectively,P<0.05).Among patients who had Hs-CRP >3mg/L,GG,and AG gene subtypes had higher percentage than A allele homozygotes(92.6%,74.2% and 45.8%,respectively.χ2=17.75,28.04,P<0.05).Conclusions This study indicated G allele of HSP70-2 gene +1267A/G polymorphism may be an independent risk factor in systemic inflammation with stable CAD.展开更多
目的 观察阿奇霉素对哮喘小鼠气道重构指标、转化生长因子-β1（transforming growth factor-β1,TGF-β1）表达的影响,探讨阿奇霉素对哮喘小鼠气道重构的影响.方法 30只雄性BALB/c小鼠随机分为正常对照组（A组）、哮喘模型组（B组）、...目的 观察阿奇霉素对哮喘小鼠气道重构指标、转化生长因子-β1（transforming growth factor-β1,TGF-β1）表达的影响,探讨阿奇霉素对哮喘小鼠气道重构的影响.方法 30只雄性BALB/c小鼠随机分为正常对照组（A组）、哮喘模型组（B组）、阿奇霉素治疗组（C组）,每组各10只,复制哮喘模型后收集支气管肺泡灌洗液（BALF）,行白细胞（TOT）,嗜酸性粒细胞（EOS）计数;医学图像分析软件观测支气管总管壁面积（Wat）、内壁面积（Wai）、平滑肌面积（Wam）;SABC免疫组化法检测肺组织TGF-β1的表达.结果 B组BALF中嗜酸性粒细胞明显高于其他组（8.12±0.54 vs 0.70±0.40,8.12±0.54 vs 0.87±0.25,P＜0.01）;C组气道Wat、Wai、Wam均较B组减轻（10.15±0.95 vs 15.36±0.85,4.16±0.32 vs 10.64±1.03,3.77±0.15 vs 7.97±0.17,P＜0.01）,但较A组加重;B组TGF-β1（168.58±21.71 vs 130.47±18.22 vs 126.30±16.15）表达最强,C组减弱,A组微弱;TGF-β1的表达与EOS%（r=0.840,P＜0.01）、Wat（r=0.735,P＜0.01）、Wam（r=0.870,P＜0.01）呈正相关.结论 阿奇霉素可抑制哮喘小鼠气道重构,可能是通过抑制TGF-β1的表达来实现的.展开更多
目的研究信号转导和转录激活因子1(signal transducer and activator of transcription1,STAT1)、信号转导和转录激活因子6(STAT6)在支气管哮喘(简称哮喘)气道炎症中的作用和地塞米松对其表达的干预。方法雄性BALB/c小鼠随机分为对照组(...目的研究信号转导和转录激活因子1(signal transducer and activator of transcription1,STAT1)、信号转导和转录激活因子6(STAT6)在支气管哮喘(简称哮喘)气道炎症中的作用和地塞米松对其表达的干预。方法雄性BALB/c小鼠随机分为对照组(A组)、哮喘组(B组)和地塞米松组(C组),每组8只。逆转录-聚合酶链反应(RT-PCR)法半定量测定肺组织中STAT1、STAT6mRNA的表达水平,组织学观察肺组织炎症程度。结果①B组肺组织中STAT1mRNA表达水平显著高于A组(P<0.01),而C组显著低于B组(P<0.01);②B组肺组织中STAT6mRNA表达水平显著高于A组(P<0.01),而C组显著低于B组(P<0.01);③C组小鼠肺组织中STAT1mRNA与STAT6mRNA的表达呈显著正相关(r=0.939,P<0.01)。结论 STAT1、STAT6的高表达参与了哮喘小鼠的病理生理过程;地塞米松可同时下调STAT1、STAT6的表达,抑制哮喘气道炎症。展开更多
文摘Objective To explore the relationship between heat-shock protein 70-2 gene +1267A/G polymorphism(HSP70-2 gene +1267A/G polymorphism) and serum level of high sensitivity C-reactive protein(Hs-CRP) in patients with coronary artery disease(CAD).Methods Serum Hs-CRP level and HSP70-2 gene +1267A/G polymorphism were detected in 185 patients with CAD.HSP70-2 gene +1267A/G polymorphism was screened by polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP).Results The genotype distribution of the HSP70-2 gene +1267A/G polymorphism was as follows: AA was in 24 of 185 patients(12.97%),AG in 93 of 185 patients(50.27%) and GG in 68 of 185 patients(36.76%).Patients with GG、AG subtype had higher Hs-CRP levels compared with carriers of the AA subtype(4.5±1.8mg/L,3.2±1.2mg/L and 2.7±1.1mg/L,respectively,P<0.05).Among patients who had Hs-CRP >3mg/L,GG,and AG gene subtypes had higher percentage than A allele homozygotes(92.6%,74.2% and 45.8%,respectively.χ2=17.75,28.04,P<0.05).Conclusions This study indicated G allele of HSP70-2 gene +1267A/G polymorphism may be an independent risk factor in systemic inflammation with stable CAD.
文摘目的 观察阿奇霉素对哮喘小鼠气道重构指标、转化生长因子-β1（transforming growth factor-β1,TGF-β1）表达的影响,探讨阿奇霉素对哮喘小鼠气道重构的影响.方法 30只雄性BALB/c小鼠随机分为正常对照组（A组）、哮喘模型组（B组）、阿奇霉素治疗组（C组）,每组各10只,复制哮喘模型后收集支气管肺泡灌洗液（BALF）,行白细胞（TOT）,嗜酸性粒细胞（EOS）计数;医学图像分析软件观测支气管总管壁面积（Wat）、内壁面积（Wai）、平滑肌面积（Wam）;SABC免疫组化法检测肺组织TGF-β1的表达.结果 B组BALF中嗜酸性粒细胞明显高于其他组（8.12±0.54 vs 0.70±0.40,8.12±0.54 vs 0.87±0.25,P＜0.01）;C组气道Wat、Wai、Wam均较B组减轻（10.15±0.95 vs 15.36±0.85,4.16±0.32 vs 10.64±1.03,3.77±0.15 vs 7.97±0.17,P＜0.01）,但较A组加重;B组TGF-β1（168.58±21.71 vs 130.47±18.22 vs 126.30±16.15）表达最强,C组减弱,A组微弱;TGF-β1的表达与EOS%（r=0.840,P＜0.01）、Wat（r=0.735,P＜0.01）、Wam（r=0.870,P＜0.01）呈正相关.结论 阿奇霉素可抑制哮喘小鼠气道重构,可能是通过抑制TGF-β1的表达来实现的.
文摘目的研究信号转导和转录激活因子1(signal transducer and activator of transcription1,STAT1)、信号转导和转录激活因子6(STAT6)在支气管哮喘(简称哮喘)气道炎症中的作用和地塞米松对其表达的干预。方法雄性BALB/c小鼠随机分为对照组(A组)、哮喘组(B组)和地塞米松组(C组),每组8只。逆转录-聚合酶链反应(RT-PCR)法半定量测定肺组织中STAT1、STAT6mRNA的表达水平,组织学观察肺组织炎症程度。结果①B组肺组织中STAT1mRNA表达水平显著高于A组(P<0.01),而C组显著低于B组(P<0.01);②B组肺组织中STAT6mRNA表达水平显著高于A组(P<0.01),而C组显著低于B组(P<0.01);③C组小鼠肺组织中STAT1mRNA与STAT6mRNA的表达呈显著正相关(r=0.939,P<0.01)。结论 STAT1、STAT6的高表达参与了哮喘小鼠的病理生理过程;地塞米松可同时下调STAT1、STAT6的表达,抑制哮喘气道炎症。
