Study On The Mechanism Of Action Of Daguomu Ginger Seed Oil In Treating Atrial Fibrillation Rats

Objective:Atrial Fibrillation(AF)is a serious hazard to human quality of life and health.CV-3 is a volatile oil extracted from the seedling medicine Cinnamomun migao H.W.Li,which has anti-arrhythmia effect.The study found that the treatment of AF is to improve the calcium ion overload in atrial myocytes.For further research,we will discuss the mechanism of action of AF in the treatment of myocardial fibrosis from CV-3.Methods:1.The optimal conditions of CV-3-β-CD were determined by orthogonal test to prepare the CV-3-β-CD.2.Eighty healthy SD rats,male and female,were selected.Rats with weight(220-300g)were randomly divided into blank group(Blank group)and model group.The tail vein was injected with Ach-CaCl2 mixture.After the model was successfully established,the model group rats were randomly divided into atrial fibrillation group(AF group),CV-3-β-CD high dose group(High dose group),CV-3-β-CD medium dose group.(Middle dose group),CV-3-β-CD low dose group(Low dose group),amiodarone group(AMD group),5 groups,continuous gavage treatment for 4 weeks,once a day during the treatment of continuous tail vein injection of Ach-CaCl2.Rat standard Ⅱ lead electrocardiograms were recorded weekly.3.After 4 weeks of gavage,the rats were sacrificed and the atrial tissue was taken.The degree of fibrosis in the atrial tissue was observed by HE staining.The atrial tissue malondialdehyde(MDA)was detected by enzyme-linked immunosorbent double antibody sandwich method(ELISA).Superoxide dismutase(SOD)levels were detected by real-time quantitative PCR(RT-PCR).The mRNA expression levels of apoptotic genes P53,P21 and P16 were detected.Results:1.The best conditions for the preparation of CV-3-β-CD:β-CD:water 1:20,β-CD:oil 1:8,temperature 60℃,high speed stirring for 50 min The saturation rate is the highest,reaching 53%.2.CV-3-β-CD can increase the body weight of rats,and the effect is better than AMD group,but the effect of reducing the duration of atrial fibrillation and lowering the ventricular rate is weaker than that of AMD group.3.CV-3-β-CD can inhibit MDA production and reduce SOD consumption,and the effect is better than AMD group.4.The mRNA expressions of P53,P16 and P21 mRNA in the model group were significantly up-regulated.CV-3-β-CD could slightly inhibit the mRNA expression of P53,P16 and P21,but weaker than the AMD group.5.CV-3-β-CD improved myocardial fibrosis to some extent,but weaker than AMD group.Conclusion:CV-3-β-CD has a therapeutic effect on Ach-CaCl2 induced atrial fibrillation in rats,which is characterized by improving living conditions,shortening the duration of atrial fibrillation,and reducing ventricular rate,which may improve the degree of myocardial fibrosis in atrial fibrillation rats by reducing the anti-oxidation of SOD consumption and inhibiting the overexpression of apoptosis genes P53,P21 and P16 mRNA.