目的研究中药升降散对脓毒症患者血清Th1/Th2失衡及相关调节因子T-bet、GATA-3的干预作用。方法将55例脓毒症患者随机分为常规组(27例)和升降散组(28例),另将健康志愿者9例设为对照组。常规组患者给予西医常规治疗,升降散组患者在西医...目的研究中药升降散对脓毒症患者血清Th1/Th2失衡及相关调节因子T-bet、GATA-3的干预作用。方法将55例脓毒症患者随机分为常规组(27例)和升降散组(28例),另将健康志愿者9例设为对照组。常规组患者给予西医常规治疗,升降散组患者在西医常规治疗的基础上加用升降散100 m L,每日2次口服或鼻饲,对照组患者予口服安慰剂;3组的疗程均为3 d。比较治疗前后3组患者中医证候评分、白细胞计数(WBC)、C反应蛋白(CRP)、降钙素原(PCT)、血清Th1/Th2及其相关转录因子T-bet、GATA-3的水平。结果常规组与升降散组比较,治疗后中医证候评分、WBC、Th1/Th2和T-bet的差异均有统计学意义(P<0.05或P<0.01),2组患者治疗后CRP、PCT和GATA3的差异无统计学意义(P>0.05);2组与对照组比较,除GATA3外,其他各项指标差异均有统计学意义(P<0.01)。结论升降散可以改善脓毒症患者中医临床征候和炎症反应指标,对血清Th1/Th2失衡及其相关调节因子T-bet、GATA-3的水平具有干预作用。展开更多
Endothelin-1 and a number of other genes expressd primarily in endothelial cells(EC)require a functional GATA element in their promoter region.The widely expressed zinc finger DNA binding protein GATA-2 has been chara...Endothelin-1 and a number of other genes expressd primarily in endothelial cells(EC)require a functional GATA element in their promoter region.The widely expressed zinc finger DNA binding protein GATA-2 has been characterized as the likely GATA factor which binds these GATA elements.To understand the specificity of this interaction,and to investigate the potential for regulation of GATA-2 activity,we have studied translation and post-translational modification of the GATA-2 protein. A specific antiserum immunoprecipitated a 52kDa GATA-2 protein from [35-S] methionine-labeled EC,as well as a wide variety of cultured human cell lines which express GATA-2 mRNA. Immunoprecipitation experiments with [32-P]-orthophosphate labeled cells indicated that GATA-2 is similarly phosphorylated in EC and non-EC lines. Thus the apparent cell-specific activity of this transcription factor is not regulated by translation or phosphorylation, and must derive from the interaction of GATA-2 with other nuclear proteins in the EC.Further studies investigated the potential regulation of GATA-2 phosphorylation in EC. Phosphoamino acid analysis indicated that GATA-2 is phosphorylated on serine and threonine residues in EC.The hasal phosphorylation of GATA-2 was rapidly and markedly increased when EC were treated with calcium ionophore A23187, while phorbol ester and forskolin had no effect.Phosphopeptide map analysis showed that A23187 induced phosphorylation of at least two additional sites in GATA-2.Gel shift assays employing nuclear extracts isolated from EC that had been treated with A23187 had a different DNA binding pattern when compared to control.This regulated phosphorylation of GATA-2 may provide a signaling pathway for hormonal regulation of endothelial cell genes such as endothelin-1 which alter their rate of transcription in response to increased intracellular calcium.展开更多
文摘目的研究中药升降散对脓毒症患者血清Th1/Th2失衡及相关调节因子T-bet、GATA-3的干预作用。方法将55例脓毒症患者随机分为常规组(27例)和升降散组(28例),另将健康志愿者9例设为对照组。常规组患者给予西医常规治疗,升降散组患者在西医常规治疗的基础上加用升降散100 m L,每日2次口服或鼻饲,对照组患者予口服安慰剂;3组的疗程均为3 d。比较治疗前后3组患者中医证候评分、白细胞计数(WBC)、C反应蛋白(CRP)、降钙素原(PCT)、血清Th1/Th2及其相关转录因子T-bet、GATA-3的水平。结果常规组与升降散组比较,治疗后中医证候评分、WBC、Th1/Th2和T-bet的差异均有统计学意义(P<0.05或P<0.01),2组患者治疗后CRP、PCT和GATA3的差异无统计学意义(P>0.05);2组与对照组比较,除GATA3外,其他各项指标差异均有统计学意义(P<0.01)。结论升降散可以改善脓毒症患者中医临床征候和炎症反应指标,对血清Th1/Th2失衡及其相关调节因子T-bet、GATA-3的水平具有干预作用。
文摘Endothelin-1 and a number of other genes expressd primarily in endothelial cells(EC)require a functional GATA element in their promoter region.The widely expressed zinc finger DNA binding protein GATA-2 has been characterized as the likely GATA factor which binds these GATA elements.To understand the specificity of this interaction,and to investigate the potential for regulation of GATA-2 activity,we have studied translation and post-translational modification of the GATA-2 protein. A specific antiserum immunoprecipitated a 52kDa GATA-2 protein from [35-S] methionine-labeled EC,as well as a wide variety of cultured human cell lines which express GATA-2 mRNA. Immunoprecipitation experiments with [32-P]-orthophosphate labeled cells indicated that GATA-2 is similarly phosphorylated in EC and non-EC lines. Thus the apparent cell-specific activity of this transcription factor is not regulated by translation or phosphorylation, and must derive from the interaction of GATA-2 with other nuclear proteins in the EC.Further studies investigated the potential regulation of GATA-2 phosphorylation in EC. Phosphoamino acid analysis indicated that GATA-2 is phosphorylated on serine and threonine residues in EC.The hasal phosphorylation of GATA-2 was rapidly and markedly increased when EC were treated with calcium ionophore A23187, while phorbol ester and forskolin had no effect.Phosphopeptide map analysis showed that A23187 induced phosphorylation of at least two additional sites in GATA-2.Gel shift assays employing nuclear extracts isolated from EC that had been treated with A23187 had a different DNA binding pattern when compared to control.This regulated phosphorylation of GATA-2 may provide a signaling pathway for hormonal regulation of endothelial cell genes such as endothelin-1 which alter their rate of transcription in response to increased intracellular calcium.
