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目的探讨单磷酰脂 A(MLA)预处理对大鼠缺血再灌注心肌的影响及环氧化酶-2(COX-2)表达的作用。方法雄性 Wistar 大鼠24只分为4组:健康对照组(NC 组)、单纯缺血再灌注组(I/R 组)、单磷酰脂 A 预处理组(MLA-DP组)、单磷酰脂 A 预处理与 COX-2抑制剂 NS-398组(MLA+NS-398组);检测各组心功能、心肌梗死的范围;测定 MLA 预处理后24 h COX-2蛋白表达及心肌中前列腺素类化合物的含量。结果与 NC 组比较,MLA-DP 组心功能明显改善[左室内压峰值(LVSP)分别为:(124.1±12.0)mm Hg和(112.0±26.3)mm Hg,P<0.01],与 MLA-DP 组比较,MLA+NS-398组心功能下降(P<0.01)、心肌梗死范围增大[分别为(14±3)%和(32±9)%,P<0.01]。与 NC 组比较,MLA-DP 组 COX-2蛋白水平明显增加(P<0.01),心肌中前列腺素类化合物含量明显增加(P<0.01)。同 MLA-DP 组比较,MLA+NS 398组蛋白水平无明显变化,但MLA+NS-398组前列腺素类化合物含量明显减少(P<0.01)。结论 MLA 预处理适度上调了心肌细胞 COX-2蛋白表达,增加心肌前列腺素类化合物前列腺素 E_2的量,从而对大鼠缺血再灌注心肌有延迟保护作用。
Objective To investigate the effects of monophosphoryl lipid A (MLA) preconditioning on myocardial ischemia / reperfusion in rats and the expression of cyclooxygenase-2 (COX-2). Methods Twenty-four male Wistar rats were divided into 4 groups: healthy control group (NC group), ischemia reperfusion group (I / R group), monophosphoryl lipid A pretreatment group (MLA-DP group) Acrolein A pretreatment and COX-2 inhibitor NS-398 group (MLA + NS-398 group); Detect the range of cardiac function and myocardial infarction in each group; measure the expression of COX-2 protein and the expression of COX- Prostaglandin compounds content. Results Compared with NC group, the cardiac function of MLA-DP group was significantly improved [LVSP] were (124.1 ± 12.0) mm Hg and (112.0 ± 26.3) mm Hg, respectively, P <0.01] In the MLA + NS-398 group, heart function decreased (P <0.01) and infarct size increased (14 ± 3% vs 32 ± 9%, P <0.01, respectively). Compared with NC group, the COX-2 protein level in MLA-DP group was significantly increased (P <0.01), and the contents of prostaglandins in myocardium were significantly increased (P <0.01). Compared with MLA-DP group, MLA + NS 398 group protein level did not change significantly, but MLA + NS-398 group prostaglandin compound content was significantly reduced (P <0.01). Conclusion MLA pretreatment moderately up-regulates the expression of COX-2 protein in cardiomyocytes and increases the amount of prostanoid prostaglandin compound prostaglandin E_2, which may have a delayed protective effect on myocardial ischemia-reperfusion in rats.