An Experimental Study Of The Effect Of Verapamil And Perdipine On Glomerular Mesangial Cell Proliferation

IntroductionGlomerular mesangial cell (GMC) is the most active inhering cell which proliferation is one ofthe most common pathologic changes in many kinds of primary or secondary glomerular disease,playing important role in glomerular sclerosis and fibrosis. The excess expression of transformgrowing factor (?)1 (TGF-(?)1) in kidney can stimulate glomerular mesangial cell proliferation, atthe same time, it is the decisive media in synthesis and fibrosis of extra cellular matrix, and itpromote the glomerular sclerosis. Peroxisom proliferators activated receptor (?) (PPAR (?) ) can beexpressed in GMC in vitro. Research has proved that PPAR (?) ligand inhibit GMC proliferation bydose-depending mode, that is to say, activation of PPAR (?) can converse GMC transformation todecrease ECM formation. So, research of the mechanism of GMC proliferation can direct clinicmedicine and treatment. Someone found that the GMC splitting can be prevented by stopping the[Ca] inflowing.ObjectiveInvestigates the inhibitory effect of calcium antagonist (CA) on glomerularmesangial cell proliferation.MethodsObserving the expression of TGF (?)1 and PPAR (?) on culturing rat glomerularmesangial cell in vitro after administrating calcium antagonist byimmunohistochemistry technique. ResultsIn the glomerular mesangial cells, TGF (?) 1 and PPAR (?) are dyed into brownparticles. verapamil and perdipine reduce the expression of TGF (?) 1 and show negativerelation to their concentration; verapamil and perdipine increase the expression ofPPAR (?) and show positive relation to their concentration.ConclusionCalcium antagonist may inhibit GMC proliferation by promote PPAR (?) expressionand reduce TGF (?) 1 expression.