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目的检测急性心肌梗死(AMI)患者外周血单核细胞环氧化酶2(COX-2)MRNA表达及其对白介素6(IL-6)分泌的影响;观察短期阿托伐他汀治疗对AMI患者外周血单核细胞COX-2MRNA表达的影响和意义。方法选取AMI患者40例(AMI组),冠心病(CHD)稳定期患者18例(对照组)。AMI患者被随机分为常规治疗组(N=20)和阿托伐他汀治疗组(常规治疗+阿托伐他汀20MG/D,N=20)治疗一周。抽取对照组及AMI组治疗前后静脉血,分离、纯化单核细胞,培养24H,其中AMI组治疗前的单核细胞培养时,采用不同浓度COX-2特异性抑制剂—塞来昔布干预(浓度分别为0、0·1、1和10ΜMOL/L)。采用逆转录聚合酶链式反应法(RT-PCR)检测单核细胞COX-2MRNA表达,酶联免疫吸附法(ELISA)测定单核细胞培养上清液中IL-6浓度和血浆中高敏CRP浓度。结果AMI组单核细胞COX-2表达(0·92±0·13)明显高于对照组(0·19±0·08)(P<0·05),经阿托伐他汀治疗一周后,其表达降低66%(与常规治疗相比,P<0·05);AMI组单核细胞培养上清液IL-6浓度为(204·8±45·6)NG/L,明显高于对照组(40·9±1·2)NG/L(P<0·05),经不同浓度的塞来昔布(0·01、1和10ΜMOL/L)体外干预培养后,10ΜMOL/L塞来昔布使IL-6浓度下降58%(与基线值相比较,P<0·05),且呈浓度依赖性;AMI组血浆CRP浓度为(43·3±14·9)MG/L,显著高于对照组(1·7±0·8)MG/L,P<0·05,经阿托伐他汀治疗后,CRP水平降低62%(与常规治疗比较,P<0·05);AMI组单核细胞COX-2表达水平与培养上清液中IL-6浓度和血浆中CRP浓度均呈正相关(R=0·636和0·662,均P<0·05)。结论AMI患者外周血单核细胞处于激活状态,单核细胞源性COX-2可能起重要的促炎作用;阿托伐他汀抑制AMI患者外周血单核细胞COX-2表达,并可能通过这一途径改善AMI的早期炎症反应。
Objective To detect the expression of cyclooxygenase 2 (COX-2) mRNA and its effect on the secretion of interleukin 6 (IL-6) in patients with acute myocardial infarction (AMI). To observe the effects of short-term atorvastatin on the expression of AMI Effect and significance of COX-2 mRNA expression in peripheral blood mononuclear cells of patients. Methods Forty AMI patients (AMI group) and 18 patients with stable coronary heart disease (CHD) were selected as the control group. Patients with AMI were randomized to receive either conventional treatment (n = 20) or atorvastatin (normol plus atorvastatin 20 MG / D, n = 20) for one week. The mononuclear cells were isolated and purified from the control group and the AMI group before and after treatment. Mononuclear cells were cultured and cultured for 24 hours. Monocytes cultured in AMI group were treated with different concentrations of COX-2-celecoxib Concentrations of 0, 0. 1, 1 and 10 MOLA / L, respectively). The expression of COX-2 mRNA in monocytes was detected by reverse transcriptase-polymerase chain reaction (RT-PCR). The concentration of IL-6 in monocyte culture supernatant and the concentration of high-sensitive CRP in plasma were detected by enzyme-linked immunosorbent assay (ELISA) . Results The expression of COX-2 in monocytes of AMI group (0.92 ± 0.13) was significantly higher than that of control group (0.19 ± 0.08) (P <0.05). One week after treatment with atorvastatin, The expression of IL-6 in monocyte-derived supernatant of AMI group was (204.8 ± 45.6) NG / L, which was significantly lower than that of control (P <0.05) (40.9 ± 1.2) NG / L (P <0.05). After in vitro intervention with different concentrations of celecoxib (0.01, 1 and 10 MOL / L), 10 MOL / Cocoxib decreased IL-6 concentration by 58% (P <0.05 compared with baseline values) in a concentration-dependent manner; plasma CRP concentrations in AMI group were (43.3 ± 14.9) MG / L, significant (1.7 ± 0.8) MG / L, P <0.05, the level of CRP decreased by 62% (compared with conventional treatment, P <0 · 05) after treatment with atorvastatin; AMI The expression of COX-2 in monocytes was positively correlated with IL-6 concentration in serum and CRP concentration in plasma (R = 0.636 and 0.662, both P <0.05). Conclusions Peripheral blood monocytes are activated in AMI patients and monocyte-derived COX-2 may play an important proinflammatory role. Atorvastatin inhibits the expression of COX-2 in peripheral blood mononuclear cells of patients with AMI and may pass this Ways to improve AMI’s early inflammatory response.