The MEK-ERK signal pathway are effected by advanced glycation end products (AGEs) in rat cardiomyocyte cell line (H9c2)

• Main Authors: Yi-Shiuan Lin, 林依萱
• Other Authors: shun-yao ko
• Format: Others
• Language: zh-TW
• Published: 2010
• Online Access: http://ndltd.ncl.edu.tw/handle/h6875j

碩士 === 長榮大學 === 醫學研究所 === 98 === One of the common chronic diseases is diabetes mellitus ( DM ), that lead various complications, include cerebrovascular disease, cardiovascular disease, retina diseases and kidney disease. The heart disease complication of diabetes is diabetic cardiomyopathy. The major problem is metabolic abnormalities may cause hardening of the arteries, myocardial inflammation, cardiac function abnormal, and leading to heart failure. In clinical setting, advanced glycation end-products ( AGEs ) accumulation and heart failure are positive correlation in DM patients. Ample evidence has suggested that AGEs accumulation increase reactive oxygen species ( ROS ) production and lead to cardiac hypertrophy. Furthermore, activation of MEK-ERK signaling regulates cardiomyocyte hypertrophy in MEK1 transgenic mice. In this study, we proposed that AGEs correlated with cell hypertrophy and affected on signal transduction pathway. We demonstrated that AGEs induced cell hypertrophy and increased the levels of total protein. Furthermore, ROS production and activation MEK-ERK were increased by AGEs. At the same time, when cell pretreated ROS inhibitor ( NAC ) the activation was blocked. This finding indicated that AGEs play an important role in heart hypertrophy through ROS to activate the MEK-ERK pathway.