论文部分内容阅读
Aim:To observe the effects of Ginkgo biloba extract(EGb)on the hypertrophy ofmesangial cells and the accumulation of extracellular matrix(ECM)in mesangialcells.Methods:Cultured mesangial cells were allotted into 7 groups:normal group,solvent control group,high glucose group,low dose of EGb group,moderatedose of EGb group,high dose of EGb group,and captopril group.Activities of cellantioxidases,S phase percentage and G_0/G_1 phase percentage,collagen Ⅳ andlaminin,Smad2/3 and Smad7,TGF-β_1 mRNA were measured by different methods.Results:For EGb-treated groups,when compared with high glucose group,thecell percentage of S phase was raised and the percentage of G_0/G_1 was lowered.The intensity of oxidative stress was weakened.The expression of Smad2/3 wasgreatly decreased and Smad7 was increased.Collagen Ⅳ,laminin and TGF-β_1mRNA were also reduced.Conclusion:EGb can suppress cell hypertrophy andthe accumulation of ECM in rat mesangial cells,which means it could play a vitalrole in the delay of glomerulosclerosis in diabetic nephropathy.
Aim: To observe the effects of Ginkgo biloba extract(EGb) on the hypertrophy of mesangial cells and the accumulation of extracellular matrix(ECM) in mesangialcells.Methods:Cultured mesangial cells were allotted into 7 groups:normal group,solvent control group,high glucose Group,low dose of EGb group,moderatedose of EGb group,high dose of EGb group,and captopril group.Activities of cellantioxidases,S phase percentage and G_0/G_1 phase percentage,collagen IV andlaminin,Smad2/3 and Smad7,TGF-β_1 mRNA was measured by different methods.Results:For EGb-treated groups,when compared with high glucose group,the cell percentage of S phase was raised and the percentage of G_0/G_1 was lowered.The intensity of oxidative stress was weakened.The expression of Smad2/3 was greatly reduced and Smad7 was increased.Collagen IV,laminin and TGF-β_1 mRNA were also reduced.Conclusion:EGb can suppress cell hypertrophy and the accumulation of ECM in rat mesangial cells, which means it could play a vitalrole in th e delay of glomerulosclerosis in diabetic nephropathy.