Deng Ping, Zhao Shui-ping, Dai Hai-ying, Guan Xian-song, Huang Hong-guang
Department of Cardiology, the Second XiangYa Hospital, Central South University, Hunan, People's Republic of China.
Clin Chem. 2006 Feb;52(2):300-3. doi: 10.1373/clinchem.2005.057893.
We examined the effect of atorvastatin on the expression of COX-2 in peripheral blood monocytes from patients with early stage of acute myocardial infarction (AMI), and the plasma C-reactive protein (CRP) concentrations were also examined.
Patients with AMI (n = 40) and with stable coronary heart disease (CHD; n = 18) were registered, and patients with AMI were randomly separated to a group that received routine therapy (group A, n = 20) or to a group that received routine therapy plus atorvastatin at 20 mg/day (group B, n = 20) for a week. Peripheral blood monocytes from patients with AMI both before and after treatment and from patients with stable CHD were isolated and cultured for 24 h. COX-2 mRNA expression was analyzed by reverse transcription-PCR. We measured concentrations of CRP in plasma by ELISA.
COX-2 expression was activated in peripheral blood monocytes from patients with AMI [0.92 (0.13)] compared with patients with stable CHD [0.19 (0.08)]; after a week of treatment, COX-2 expression in group B (reduced by 66%) was obviously lower than in group A (reduced by 24%; P <0.05). Plasma concentrations of CRP from patients with AMI [43.3 (14.9) mg/L] were increased compared with those from patients with stable CHD [1.65 (0.78) mg/L; P <0.05]; after a week of treatment, CRP concentrations in group B (reduced by 62%) were lower than in group A (reduced by 35%; P <0.05). COX-2 expression in peripheral blood monocytes from patients with AMI was positively correlated with plasma CRP concentration (r = 0.662; P <0.05).
COX-2 may promote acute inflammatory process after AMI. Atorvastatin may improve the antiinflammatory effects through the COX-2 pathway.
我们研究了阿托伐他汀对急性心肌梗死（AMI）早期患者外周血单核细胞中COX-2表达的影响，并检测了血浆C反应蛋白（CRP）浓度。
纳入AMI患者（n = 40）和稳定型冠心病（CHD；n = 18）患者，将AMI患者随机分为接受常规治疗的组（A组，n = 20）或接受常规治疗加20 mg/天阿托伐他汀的组（B组，n = 20），治疗一周。分离并培养AMI患者治疗前后及稳定型CHD患者的外周血单核细胞24小时。通过逆转录聚合酶链反应分析COX-2 mRNA表达。我们通过酶联免疫吸附测定法测量血浆中CRP的浓度。
与稳定型CHD患者[0.19（0.08）]相比，AMI患者外周血单核细胞中的COX-2表达被激活[0.92（0.13）]；治疗一周后，B组中COX-2表达（降低66%）明显低于A组（降低24%；P<0.05）。AMI患者的血浆CRP浓度[43.3（14.9）mg/L]高于稳定型CHD患者[1.65（0.78）mg/L；P<0.05]；治疗一周后，B组中CRP浓度（降低62%）低于A组（降低35%；P<0.05）。AMI患者外周血单核细胞中的COX-2表达与血浆CRP浓度呈正相关（r = 0.662；P<0.05）。
COX-2可能促进AMI后的急性炎症过程。阿托伐他汀可能通过COX-2途径改善抗炎作用。
