摘要
目的 探讨L 肉毒碱 (L carnitine ,L Car)对缺氧 复氧培养新生大鼠心肌细胞能量生成的影响及其机制。方法 以原代培养新生大鼠心肌细胞建立缺氧 复氧损伤模型 ,高效液相色谱检测单纯缺氧 复氧以及L Car预处理缺氧 复氧心肌细胞ATP、ADP、AMP生成改变 ;RT PCR方法检测心肌细胞肉毒碱脂酰基转移酶 Ⅱ (carnitinepalmitoyltransferase Ⅱ ,CPT Ⅱ )mRNA表达。结果 与正常对照组比较 ,培养心肌细胞缺氧 2 4h复氧 0、2、4、8h后 ,心肌细胞ATP、ADP均明显下降。与单纯缺氧 复氧组比较 ,L Car预处理组心肌细胞缺氧 复氧后ATP含量明显增高 ;培养心肌细胞缺氧 2 4h后 ,CPT ⅡmRNA表达除复氧 2h有所上升外 ,复氧 4、8h表达渐次降低。L Car预处理使缺氧 2 4h复氧 4h心肌细胞CPT ⅡmRNA表达呈浓度依赖性增高 ,5 0nmol L处理组CPT ⅡmRNA表达显著高于 0nmol L处理组。结论 心肌细胞缺氧 复氧过程中能量生成明显降低 ,其损伤可能与三羧酸循环中呼吸酶CPT Ⅱ表达降低有关 ;L Car对培养仔鼠心肌细胞缺氧复氧损伤具有显著保护作用 ,其机制可能是与L Car从转录调控水平改善CPT Ⅱ合成有关。
Objective To investigate the effects of L carnitine (L Car) on the energy production in cultured neonatal rat myocardial cells after hypoxia/reoxygenation (H/R) and its mechanisms. Methods An H/R injury model was established using primary cultured rat myocardial cells. ATP, ADP and AMP contents in simple H/R treated cultured myocardial cells and L Car pretreated group were determined by high performance liquid chromatography. Carnitine Palmitoyltransferase Ⅱ (CPT Ⅱ) mRNA expression in cultured myocardial cells was detected by RT PCR. Results Compared with those in the control, ATP and ADP contents decreased significantly after 24 h hypoxia followed by reoxygenation for 0, 2, 4 and 8 h. Compared with that in simple H/R group, ATP content increased significantly in L Car pretreated group. CPT Ⅱ mRNA expression in cultured myocardial cells increased slightly after hypoxia followed by reoxygenation for 2 h, but it decreased at 4 and 8 h after reoxygenation. CPT Ⅱ mRNA expression in cultured myocardial cells pretreated with L Car at 24 h followed by reoxygenation for 4 h increased in a dose dependent manner. CPT Ⅱ mRNA expression in cultured myocardial cells pretreated with L Car at the dose of 50 nmol/L was significantly higher than that at the dose of 0 nmol/L. Conclusion H/R results in suppressed energy production in cultured myocardial cells. The possible mechanism may be associated with the down regulation of CPT ⅡmRNA expression. L Car has protective effect on the H/R induced injury of cultured neonatal rat myocardial cells, and its mechanism might be involved in the improvement of CPT Ⅱ synthesis at the transcriptional level.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2004年第3期201-204,共4页
Journal of Third Military Medical University
基金
国家重点基础研究发展规划项目 ("973"项目 ) (G19990 54 2 0 2 )~~
