Effects Of Aralosides To Adhesion Molecules Expression During Rat Myocardial Ischemia Reperfusion

Back Ground and Objective:In nowadays,coronary heart disease(CHD) was the important cause of adult's death.It is in the first place of all kinds of dead causes in developed countries of economics and industrialization.The incidence rate and mortality of CHD are lower in our country than those countries,but with the development and changes of the society and economics,the incidence rate of CHD is in rising tendency year by year in most of regions,espicaliy in north and developed regions.So the prevention and cure of cardiovascular disease has been the important researchful subject of medicine in each country.MIRI are the common clinical pathology phenomenon,the pathophysiology foundation of the myocardial infarction in coronary heart disease.Adhesion molecule has closely related to MIRI.Variety of adhesion molecules have been more and more attetion in myocardial ischemic/reperfusion injury.And CD40 / C D40L P-selectin are the hot research points in recent year.As a important constitution of world-medicine,it is the main researchful direction of traditional Chinese medicine(TCM) of using wildings to treat disease and developing effective new drugs to prevent and cure chest pain,at present. CHD belongs to the"chest pain"or"heartache"category in TCM.Deficiency in origin and excess in superficiality and simultaneous occurrence of deficiency and excess syndromes is its main pathogenesis.Excess in superficiality are cold retained,qi stagnation,blood stasis and obstruction by phlegm.Deficiency in origin are deficiency of qi,blood,yin and yang.Deficiency of heart-qi is the essence of onset of disease and the key of pathogenesis.Qi can't promot circulation of blood because of deficiency of heart-qi,which leads to blood vessels stasis.Blood stasis due to qi deficiency is the most common pathogenesis of CHD. This subject aims at this pathogenesis,uses the method of supplementing qi and activating blood to treat CHD,observes the effect of Aralosides on myocardium ischemic reperfusion injury.Aralosides possess the capabilities of anti-inflammatory,anti oxygen free radicals and anti myocardial ischemic.The study was performed by using myocardial I/R model to investigate the effects of Aralosides and Propranolol on expression of adhesion molecules in rats after myocardial ischemia/reperfusion injury.Methods and Results:Partâ… :To investigate effects of Aralosides to the quantity of P-sel expression on endocardium during myocardial ischemia reperfusion.Methods:A model of myocardial ischemia 45min followed by 5min reperfusion was made by reversibly ligating coronary left descending artery.P-sel were observed.As a result, Aralosides has no significant effect of the quantity of P-sel expression.Partâ…¡:To investigate the effects of Aralosides on expression of inflammatory molecule ICAM-1 and the activity of Malcic Dialdchyde(MDA) & Glutathione Peroxidase(GSH-PX) in rats after myocardial ischemia/reperfusion(MI/R) injury. Methods:A model of myocardial ischemia 45min followed by 6h reperfusion was made by reversibly ligating coronary left descending artery.30 Wistar rats were divided randomly into 3 groups:Ichemia reperfusion Group,Aralosides Goup, Plavix Group.HE staining was used to observe the pathological changes of myocardial issues.The activity of MDA and GSH-PX was measured,too.ELISA was used to determine ICAM-1 expression in myocardium.Results:In rats treated by Aralosides or Plavix,the lactate dehydrogenase LDH) activity was significantly decreased.Meamwhile,Aralosides and Plavix raised the activity of Malcic Dialdchyde(MDA) & Glutathione Peroxidase(GSH-PX).ICAM-1 expression was detected in myocardium after ischemia 45min followed by 6h reperfusion.In rats treated by Aralosides or Plavix,ICAM-1 expression remained unchanged.Partâ…¢:To investigate the effects of Aralosides on Mortality of rat model with myocardial infarction Methods.Mcthods:43 Wistar rats were divided randomly into 4 groups:ischemia reperfusion group(n=11),Aralosidcs group(n=10), Propranolol group(n=12),Diltiazem group(n=10).The left anterior coronary descending artcry was ligated for 45 min.ECGs werc recorded incessantly during myocardial ischemia.Thc ECG was analysed and given score in Lambeth regulation.The occurrence rate of repcrfusion arrhythemia(VF) was analyscd.Rcsults:In rats treated by Aralosides,the occurrence rate of repcrfusion arrhythemia(VF) showd no difference.However,mortality was significantly decreased.Partâ…£:To investigate effects of Propranolol to the quantity of CD40Lexpression on endocardium during myocardial ischcmia reperfusion.Methods:A model of myocardial ischemia 45min followed by 5min reperfusion was made by reversibly ligating coronary left descending artery.As a result,Propranolol reduced the quantity of CD40L expression significantly.Conclusion:1.Aralosides could protect myocardium from inflammatory injury during MI/R. Aralosides has no significant effect of P-sel,ICAM-1.The mechanism is related to the enhancement of antioxidative effect on cells,and the reduction membrane damage caused by free radical and lipid peroxide.2.Propranolol reduced the quantity of CD40L expression significantly during MI/R.This was a new mechanism of their pharmacologic action and as a proof for them to be applied to ACS.3.Mortality of rat model with myocardial infarction could significantly decreased in rats treated by Aralosides.The mechanism may be related to that Aralosides could protect myocardium from injury during MI/R.