PGC-1α在慢性间歇性低压低氧适应心脏保护中的作用及机制

慢性间歇性低压低氧(chronic intermittent hypobaric hypoxia, CIHH) 具有明显的心脏保护作用, 可增强心肌抗缺血/再灌注损伤的抵抗力。心脏的正常结构和功能有赖于能量代谢的稳定，能量代谢紊乱是心肌缺血/缺氧损伤的重要原因，优化心肌能量代谢是目前抗心肌缺血、心脏保护研究的焦点之一。PGC-1α是心脏能量代谢的关键调节分子，是机体各种代谢通路的"分子开关"，在心脏生理和病理生理过程中发挥着重要的作用。心肌缺血时心脏中PGC-1α的表达减少，而PGC-1α表达增加可明显增强心脏耐受缺血、缺氧的能力。有关PGC-1α在CIHH心脏保护中的作用未见报道。本研究旨在通过功能学、形态学、生物化学及分子生物学等方法，探讨PGC-1α在CIHH心脏保护中的作用及其机制。该研究将为心脏缺血性疾病的预防、治疗提供新的内容和思路，具有重要的理论意义和潜在的应用价值。

Chronic intermittent hypobaric hypoxia（CIHH）has cardiac protection against ischemia/reperfusion (I/R) injury. The normal structure and function of the heart depend on stabilization of energy metabolism, and disturbance of energy metabolism may contribute to I/R injury. Therefore, optimization of cardiac energy metabolism will provide a new strategy to protect ischemic heart disease. PGC-1α is a key regulatory factor involved in energy metabolism by acting as the "energy switch", which plays an important role in cardiac physiology and patho-physiology. Expression of PGC-1α is decreased in ischemic heart, while increase of PGC-1α expression in heart would enhance the endurance of heart to ischemia and hypoxia. However, the effect of PGC-1α in CIHH cardiac protection has not been reported yet. The aim of present study is to investigate the role of PGC-1α in CIHH cardiac protection and underlying mechanism by using functional, morphological, biochemical, and molecular biological methods. The study will provide new evidence and concept for prevention and treatment of ischemic heart disease, which possesses an important significance theoretically and a potential applying value clinically.