机构地区:[1]DepartmentofClinicalPharmacology,ChinaMedicalUniversity,Shengyang110001,China
出 处:《Acta Pharmacologica Sinica》2004年第1期35-40,共6页中国药理学报(英文版)
基 金:ProjectpartlysupportedbytheKeyFoundationoftheMinistryofPublicHealthofChina,№88402257.
摘 要:AIM: To study the effects of dl-praeruptorin A (Pd-Ia) on nucleus factor-κB (NF-κB) activativity and tumor necrosis factor-α(TNF-α)expression in ischemia-reperfusion (I/R) myocardium. METHODS: Langendorff's isolated rat heart was subjected to a 10-min ischemia followed by a 30-min reperfusion. NF-κB activity in nucleus was analyzed by Sandwich Enzyme-Linked Immunosorbent Assay (ELISA). TNF-α level in cytoplasm was measured by radioimmunoassay. Infiltration of neutrophils was observed using Hematoxylin-Eosin staining under optical microscope. RESULTS: Pd-Ia 1.0 μmol/L with 30-min preventive perfusion decreased NF-κB activity from 0.98±0.13 to 0.65±0.17 (P<0.05 vs solvent) and down-regulated TNF-α expression from 13.7±6.1 ug/L to 9.4±2.7 μg/L (P<0.01 vs solvent) under conditions with increase of coronary flow, negative inotropic action, inhibition of creatine kinase and without chronotropic action, whereas, infiltration of neutrophils was mild. CONCLUSION: Pd-Ia inhibited NF-κB activativity in I/R myocardium and led to down-regulation of TNF-α expression, which might be one of molecular mechanisms of Pd-Ia in cardioprotection.AIM: To study the effects of dl-praeruptorin A (Pd-Ia) on nucleus factor-κB (NF-κB) activativity and tumor necrosis factor-α(TNF-α)expression in ischemia-reperfusion (I/R) myocardium. METHODS: Langendorff's isolated rat heart was subjected to a 10-min ischemia followed by a 30-min reperfusion. NF-κB activity in nucleus was analyzed by Sandwich Enzyme-Linked Immunosorbent Assay (ELISA). TNF-α level in cytoplasm was measured by radioimmunoassay. Infiltration of neutrophils was observed using Hematoxylin-Eosin staining under optical microscope. RESULTS: Pd-Ia 1.0 μmol/L with 30-min preventive perfusion decreased NF-κB activity from 0.98±0.13 to 0.65±0.17 (P<0.05 vs solvent) and down-regulated TNF-α expression from 13.7±6.1 ug/L to 9.4±2.7 μg/L (P<0.01 vs solvent) under conditions with increase of coronary flow, negative inotropic action, inhibition of creatine kinase and without chronotropic action, whereas, infiltration of neutrophils was mild. CONCLUSION: Pd-Ia inhibited NF-κB activativity in I/R myocardium and led to down-regulation of TNF-α expression, which might be one of molecular mechanisms of Pd-Ia in cardioprotection.
关 键 词:dl-praeruptorin A MYOCARDIAL ISCHEMIA reperfusion injury nucleus factor-κB tumor necrosis factor-α
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