The Experimental Study Regulation Effect Of Compound Astragalus Nourishing Heart Mixture On The Rat Of Atrial Fibrillation About CTGF And Atrial Structural Remodeling

Objective To observe the function of Compound Astragalus Yangxin mixture in the treatment of atrial fibrillation. Also investigating the mechanism of atrial fibrillation especially the regulation of CTGF, and provide an experimental basis for the clinical application.Method The successfully established experimental atrial fibrillation rats models were randomly divided as irbesartan group and Chinese medicine high, medium and low dose group group with 10 rats in each group. By intravenous injection of calcium chloride-acetylcholine solution making rat model of atrial fibrillation (including CaC12 10 mg/mL, Ach 66 μg/mL),the dose is 1ml mixture per 100g rat weight. Once a day, and a total of 4 weeks. Normal group was given equal normal saline tail intravenous injection. After 4 weeks,starting drug lavage solution, once a day. After 8 weeks, all rats were taken blood from their abdominal aorta, also atrial tissues were taken. CTGF、TGF-β1、HGF accumulation in the serum were measured by ELISA. CTGF, TGF-β1, HGF analysis in the Atrial tissue were semi-quantitatively measured by western bolt.Results The serum CTGF、TGF-β1 content of the three Chinese medicine groups and Irbesartan group are less than the model group (P<0.05),and the HGF level of Chinese medicine group and irbesartan group is higher than the model group(P<0.05). The content of atrial CTGF and TGF-beta 1 form Chinese medicine group and irbesartan group is less, and HGF levels of the two groups was increased, but only Chinese medicine medium group CTGF TGF-β1 was significant lower in the model group (P<0.05), and HGF was significant higher than the model group (P<0.05), but not as well as the normal group.Conclusion Compound Astragalus nourishing heart mixture may inhibit mitogen-activated protein kinases,(MAPKs) signal pathway phosphorylation of expression,and inhibitory effect on rapid adhesion cells and nicotinamide adenine dinucleotide phosphate oxidase and inhibiting the production of CTGF, thus inhibiting the atrial fibrosis, playing a role in the treatment of atrial fibrillation.