Ischemic heart disease (IHD) is a group of heart diseases which include acute myocardial infarction, atherosclerosis and other coronary heart diseases. Ischemic heart disease is kind of a major chronic noninfectious disease and critical cause of death among chronic noninfectious diseases. 24 million people died of chronic noninfectious disease each year, in which 7.2 million people died of IHD, according to a report from WHO in 1997. The mechanism of Myocardial cell injury during ID may relate to a series of irreversible pathological alterations. Therefore. the exploitation of naturally occurring drugs may provide new approach that can be effective in the treatment of ischemic heart disease. Total flavonoids extract from leaves of natural plant Crataegus pinnatifida (hawthorn) possesses a wide range of pharmacological properties. However, little is known about the protective mechanism by which total flavonoids from leaves of Crataegues pinnatifida (TFFLOCP) exert cytoprotective effect in myocaridac cells from oxidative injury. This study focused on the protective mechanism of on H2Oz-induced injury of H9c2. The appropriate apoptosis-inducing condition was investigated first. We found 150 uM H202 after incubation of 24hours may achieve the optimized condition for inducing apoptosis of H9c2 cells. Different concentration of TFFLOCP and different incubation time have been investigated by our previous study. Pretreatment of myocardiac H9c2 cells with different concentration groups of TFFLOCP (100ug/ml, 200ug/ml) showed significant effects in preventing oxidative stress injury by exposuring cells in 150umol H202 for 24 hours vs. control group. Further study indicated TFFLOCP prevented H202-mediated ROS generation and maintained normal mitochondrial membrane potential. The activity of capase-3 was also inhibited in comparison to control group. Finally, we proved that high concentration group of TFFLOCP may exert strong protective effects in myocardic H9c2 cells against H202-induced oxidative injury via modulation of ROS generation, maintenance of mitochondrial membrane potential and inhibition of caspase-3 activity.

缺血性心臟病(簡稱IHD）是一類心臟疾病的總稱，其中包括急性心肌楰 賽、動脈粥樣硬化和其他冠狀心臟疾病。缺血性心藏病是一頫主要的慢性非傅染性疾病,並且也是慢性非傅染性疾病的主要致死原因。據WHO的官方報導，1997年全球有2400 百萬人死於非傅染性疾病，其中缺血性心臟病占 720 萬。缺血性 心藏病中常會件隨有心肌細胞的損傷，其損傷機制车沙到一系列不可逆的病理改變。因此探索治療缺血性心臟病的天然藥物具有潛在的意義。 來自山楂 (Crataesus pinnatifida）藥中的總黄酮具有很多藥理作用。然而我們對山楂 (Crataegus pinnatifida）葉總黄酮是如何對抗由氧化應激所導 致心肌細胞損傷的保護機理简不清楚。該研究主要集中在探討關於山楂 (Crataegus pinnatifida）葉總黃酮對於對抗由 H0.水所致的心肌細胞 H9c2 損 傷的保護機理。我們發現 150RM1 H0，連續作用 24 小時可以取得穩定的誘導細胞 调亡的效果。同樣我們考察了不同的山楂 ( Crataegus pinnatifida）葉總黃酮 的作用時間及濃度，我們發現與對照組相比，100ug/ml， 200ug/ml 的山楂 Crataegus pinnatifida）葉總黄酮預處理可以取得顯著的對抗由 150M1 Hi0z 連續作用 24 小時所帶來的氧化應激損傷，進一步的研究表明山楂 (Crataegus pinnatifida）葉總黃酮可以抑制由 H0,所引起的ROS 的釋放以及 caspase-3活 性的升高。 基於上述的實驗我們認爲高濃度組的山楂 (Crataegus pinnatifida）葉總 黄酮可能通過調節 ROS 的產生、維持線粒體膜電勢以及抑制 Caspase-3的活性來 對抗由 H0，所誘導心肌細胞 H9c2 氧化應激損傷。