The Ameliorated Effects Of Oxymatrine/Aspirin Against The Cardiac Fibroblast Proliferation Induced By Aldosterone In Vitro

Objective To clarify the gene signal regulation in cardiac fibroblastproliferation induced by aldosterone, and then to investigate the ameliorated effects ofOMT/Asp and regulated JNK and ERK signal pathway, for OMT/Asp therapeuticcardiac fibrosis providing the novel experimental data. Methods Cardiac fibroblastswere isolated and purified from1-3days SD suckling rat with trapsin digestion anddifferential adhesion. The cardiac fibroblast was authenticated byimmunofluorescence method with vimentin protein staining, and the morphologicalchange was observed with inverted microscope. The optimal concentration and timeof ALD induced cardiac fibroblast abnormal were explored by MTT methods. Theexperiment was divided into7groups as following: control (treated with DMECmedium), model (expose to ALD1×10-7mol/L), OMT two groups (preincubated with7.57×10-4mol/L and3.78×10-4mol/L,respectively, and then expose to ALD1×10-7mol/L), Asp group (Preincubated with Asp1.11×10-6mol/L, and then exposed toALD1×10-7mol/L), TGF-βblocker group (Preincubated with Alk51.5×10-5mol/L,and then exposed to ALD1×10-7mol/L),and Spironolactone group (Preincubated withSpironolactone1×10-6mol/L, and then expose to ALD1×10-7mol/L). The mRAN andprotein expression of JNK, ERK, and Akt1were detected by fluorescence realtime-PCR and western blotting. Results Exposed the cardiac fibroblast to ALD, theMMT volume significantly increased, and OMT/Asp could inhibit the cardiacfibroblast proliferation induced by ALD. Further research confirmed that OMT/Aspalleviated the mRNA and protein expression of JNK, ERK, Akt1of cardiac fibrosis byreal time-PCR and western blotting. Conclusion Aldosterone can regulate the ERK,JNK, and Akt1in MAPK/ERK and JNK signal pathway of cardiac fibroblast proliferation induced by ALD. The OMT and Aspirin ameliorate the cardiac fibrosisinvolving in inhibited ERK and JNK expression.