The Research Of Statins' Protection With The Infarct-myocardium Of The Acute Myocardial Infarction

Because of the excellence precaution and treatment for cardiovascular disease, Statins now be to focus everyone's attention upon, especial it's pleiotropia except about of degrading cholest. To study and research the protection of the laster significant Rosuvastatin is more important. Rosuvastatin has been given approval in American on Augest at 2003, has been entered China in 2005, has a Chinese name可定. For its polar-methylsulfonyl, so that it has hadro- hydrophilism. and better lower- sulfatide effectiveness. And it has the resemble kak- event. For its super- effective short, having no sexuality difference and agesensitivity, Medication time has no-circumscribe,it has been to favor. Acute myocardial infarction is looked for inflammation, and the first 24-houre is considered to be danger, there are a lot of cell factors in myocardium and blood, the early inflammation can aggravate the risk of AMI. SO thart experts show solicitude for how and why statin can antagonize the inflammaton. In 1995, the first time, Japanese scholar discovered Interleukin-18, it is a multi-efficacy ante-; inflammatory-factor., and has a core player with the waterfall-explosion of inflammatory reaction, and with the priming and development of the immune reaction. The evid of clinical research indicated, IL-18 have be higher in CDH patients than others, but the highist in ACS patients. But The evidence of infarctus-myocardium are less, and propter -less the Rosuvastatin. Cyclooxygenase-2 is the rate-limiting enzyme of prostaglandins, and has be responder- gene.play a important pole in inflammatory-factor.COX-2 is a derivned-enzyme, and seldom express with normal tissue. And some animal test indicated, COX-2 immunological activity has been accentuation in the infarctus cells, blood vessel endothelium celles and macrophages of the myocardial infarction after 2-weeks,. And in clinical research, scholars discovered that the atorvastatin.could inhibit the COX-2-expression of the histomonocyte in peripheral blood of ACS patients. At present, there is no sure report of inhibiting the COX-2-expression in necrosis cells of the earlier myocardial infarction with Rosuvastatin Now, we design the experiment to observe the chang of IL-18mRNA and COX-2mRNA with the Acute Myocardial Infarction(AMI) Rat, and to approach the protection of Rosuvastatinamd the possible mechanism.Methods: With 100 healthy 230-240g Wistar rats,50 female, and 50 male,,(come fom animal experiment centre of the foundation college of Jilin university), have trabant average 5 groups, A group: control group. B group: acute myocardial infarction group, C group: 3-days before AMI with Rosuvastatin 20mg/kg d intragastric administration, D group: 4-hours after AMI with Rosuvastatin 20mg/kg d intragastric administration, E group: 12-hours after AMI with Rosuvastatin 20mg/kg d intragastric administration.A group and B group give 3days with isotonic Na chloride 20mg/kg d. Make manufacture myocardial infarction analog with disclosing breast of the rat, and reveal the anterior descending coronary. To anesthetize rats with vinic ether, after OK, make tracheostomy tube, link small animal breathing; vent, open the chest and milking the heart, then, with 7-0 ophthalmology-sewing-needle suturing the ramus descendens anterior arteriae coronariae sinistrae,which is 3mm distance with aortic root between auricula atrii sinistri; auricula sinistra and pulmonary conus. sham operation have no ligation. For avoidancing the influence to white cell count, we application no-anti-inflammatory. After 24hours of ligation anterior descending coronary artery, obtain no- anticoagulation blood 3ml to measure WBC-enumeration, 2ml blood to survey CK and LDH. The weigh heart. Measuring infarct size with N-BT. Myocardium sample homogenate, determined IL-18mRNA and C0X-2mRNA with RT-PCR, then doing agarose gel electrophoresis. Other hearts were conserved infarctus campus of aortic ventricle in 10% neutro-formalin for 24hours, then make manufacture paraffin envelop lump, the slices hasve been done HE dyeing.Results:Compared with unadministered rats, administer with Rosuvastatin lowered infarct size, plasmic CK, LDH, lencocyte count were degraded(p<0.05). COX-2mRNA and IL-18mRNA of control group have been lightly expressed, these in AMI group have been expressed at most. Medication every group: before AMI given group, the IL-18mRNA and COX-2 mRNA have been least expressed (p<0.01). IL-18mRNA in 12hours given group have been higher than 4hours given group (p<0.05); and COX-2 in after AMI given groups have been lessen expressed(p<0.05), but have been no-difference (p>0.05).Conclusions: IL-18 and COX-2 can been monitoring indicatrixes after AMI. Statins have anti-inflammatory effect. Rosuvastatin could protect AMI heart by oppositeing inflammation with decreaseing the expression of IL-18 and COX-2;We should give ACS patients statins as posseble as quikely.