重症急性胰腺炎与心肌细胞凋亡

重症急性胰腺炎时可明显导致心肌损害,心肌细胞凋亡也会明显增加,其程度随着心肌损害程度的加重而加重,同时随着重症急性胰腺炎病程的延长而逐渐加重。本文主要综述了心肌细胞凋亡的调控基因,占有非常重要地位是Bcl-2基因家族,其中Bcl-2基因和Bax是一对功能完全相反的重要的细胞凋亡调节基因,参与了抑制或诱导细胞凋亡。两者的比例调节着细胞凋亡的发生,决定着细胞是存活还是凋亡;重症急性胰腺炎导致心肌细胞调亡的可能机制以及重症急性胰腺炎时诱导心肌细胞凋亡的治疗。当细胞凋亡为细胞死亡的主要方式时,通过积极有效的药物干预,有可能逆转过度凋亡所致的病理变化,减少细胞凋亡,促进细胞再生。故进一步研究重症急性胰腺炎细胞凋亡基因调控以及细胞凋亡基因信号传导途径,必将为全面了解急性胰腺炎和胰心综合症的发病机制提供科学依据,为研究有关治疗药物的作用机制开辟崭新的前景。

Advance on the relationship between severe acute pancreatitis and cardiac myocytes apoptosis

Severe acute pancreatitis （SAP） can obviously lead to myocardium damage and myocardial cell apoptosis also will be significantly increased. The extent of damage of the myocardial cell apoptosis aggravates along with the myocardial injury and at the same time, aggravates with the disease course too. This paper mainly reviewed the very important regulation gene of the myocardial cell apoptosis, the Bcl-2 gene families, including Bcl-2 gene and Bax gene. Their functions are completely opposite, involving in inhibiting or inducing cell apoptosis. The proportion of the two regulates the cell apoptosis happen, determines that the cell is whether survival or apoptosis. This paper also reviewed the possible mechanisms of myocardial cell apoptosis caused by SAP and the treatment of the induced myocardial cell apoptosis in SAP. When the cell apoptosis is the main way of the cell death, it might reverse the pathological changes caused by excessive apoptosis, reduce the cell apoptosis and promote the cell regeneration by the active and effective drug intervention. Therefore, it will provide the scientific basis for a comprehensive underst＇~/nding of the pathogenesis of acute pancreatitis and pancreatitica-heart syndrome and open up a new prospect for research on the mechanism of drug treatment that further study on the cell apoptosis regulation genes and their signal transduction pathways in SAP.