中文摘要：

目的观察心痛舒合药血清预处理对缺氧／复氧乳鼠心肌细胞核因子-KBp65（NF—KBp65）及其下游调控因子肿瘤坏死因子-α（TNF—α）、白介素-1β（IL-1β）的影响，探讨心痛舒对心肌细胞缺氧／复氧损伤的保护作用机制。方法原代培养SD乳鼠心肌细胞，建立模拟心肌细胞缺氧／复氧损伤模型，设正常组、模型组、阳性对照组、心痛舒含药血清预处理组共4组。罗丹明B染色法观察心肌细胞形态，ELISA法测定培养液上清TNF—α、IL一1β含量，半定量RT—PCR方法检测NF—KBp65mRNA表达水平。结果与模型组比较．阳性对照组、心痛舒含药血清预处理组TNF一α、IL，-lβ水平降低，NF—KBp65mRNA的表达水平下降，差异有统计学意义（P〈0．01）；与阳性对照组比较心痛舒含药血清预处理组NF—KBp65mRNA表达降低，差异有统计学意义（P〈0．05）。结论心痛舒含药血清预处理可通过抑制缺氧一复氧心肌细胞炎症反应途径发挥保护作用，其机制与抑制NF—KB活化，从而抑制下游炎性细胞合成有关。

英文摘要：

Objective To observe the regulating effects of preconditioning with serum containing Xintongshu on the expression of nuclear factor-KBp65 （NF-KBp65）, tumor necrosis factor-α（TNF-α） and interleukin-lβ（IL-lβ）, and to explore the protective mechanism of Xintongshu on the hypoxia and reoxygen injury myocardial cell model of newborn rat. Methods The myocardial cells were isolated from neonatal rats and cultured,then modelled with hypoxia andreoxygenation injury. The modeled myocardial ceils were randomly divided into tour groups, mcmo ing normal control group, model control group, positive control group and preconditioning group treat- ed with serum containing Xintongshu （Xintongshu group）. The myocardial cell morphologic changes were observed by Rhodamine B stain. The TNF-α and IL-ll5 proteins in culture media were detected by ELISA and the mRNA expression level of NF-KBp65 was detected by RT-PCR. Results Compared with model control group,the expression levels of TNF-α and IL-1β proteins and NF-KBp65 mRNA in positive control group and Xingtongshu group were decreased. There were sta- tistical differences （P〈0.01）. Compared with positive control group, the expression levels of NF- KBp65 mRNA in Xingtongshu group were statistically decreased （P〈0.05）. Conclusion The precondi- tioning with serum containing Xintongshu can exert a protective effect by inhibiting the inflammatory reaction pathway of the hypoxia and reoxygenation myocardial cells. The effect may be related to the decrease of the NF-KB p65 mRNA expression level and further inhibition of thegeneration of in- flammatory cells.