Purpose　To study the effects of α-tocopherol on activator protein-1(AP-1)binding and TGF-β1 expression induced by high glucose in rat mesangial cells and further to clarify the molecular mechanism of antioxidant in treating diabetic nephropathy.　Methods　AP-1 binding of the rat mesangial cells exposed to high glucose was detected by gel shift assay.The Jun,Fos compositions of AP-1 dimer were determined by supershift assay.Protein expression of TGF-β1 was detected by Western blot.Additionally,the effects of α-tocopherol on AP-1 binding and TGF-β1 expression induced by glucose in rat mesangial cells were also studied.　Results　High glucose stimulated AP-1 binding of mesangial cells in time-and-dose-dependent manners .This AP-1 binding increase involved JunD and Fos as shown by gel supershift.Glucose also increased protein expression of TGF-β1 at same time.The increased AP-1 binding and TGF-β1 were inhibited with pretreatment with α-tocopherol in glucose-treated mesangial cells.　Conclusions　This study suggests that α-tocopherol can significantly inhibit AP-1 activity and TGF-β1 expression by glucose in rat mesangial cells,which may be one of its antioxidation mechanisms to retard diabetic nephropathy.

Objective: To investigate the therapeutic efficacy and mechanisms of ?-sodium aeacine in treating chest trauma.Methods: One hundred and sixty patients with chest trauma were randomly divided into two groups: the control group and the study group.The control group was treated by conventional method,while in addition to the conventional treatment,the study group was also treated with ?-sodium aeacine,10 mg of ?-sodium aeacine in 250 ml 10% glucose solution for intravenous drip,30 to 40 drops/min,twice a day for 10 days(one therapeutic course).Results: The effective and total effective rates of the study group were significantly higher than those of the control group(the effective rate(62.5% vs.22.5%) and the total effective rate(97.5% vs.66.3%),both P