Event Title
Location
Philadelphia, PA
Start Date
8-5-2019 1:00 PM
End Date
8-5-2019 4:00 PM
Description
Advanced glycation end (AGE) products have been under investigation for their role in cardiovascular disease in complications. Methylglyoxal, a byproduct of glucose metabolism, is elevated in the blood of diabetic patients and has shown to be an important intermediate in the production of AGEs. Due to the highly reactive structure of methylglyoxal, it can produce high levels of reactive oxygen species (ROS) within the cell via mitochondrial modification which results in a loss of cell membrane potential and possible cell death. The role of methylglyoxal in cardiac cells is not well known; in this study methylglyoxal induced cell injury and ROS generation were investigated by co-treatment of methylglyoxal with metformin, aminoguanidine hydrochloride, or pyridoxamine dihydrochloride. The effects of methylglyoxal on H9C2 myoblast viability were evaluated after incubation of drugs for 24 hours by measuring absorbance at 450 nm by using tetrazolium to differentiate metabolically active and inactive cells (e.g., CCK-8 kit). We found that methylglyoxal (1200 µM) significantly reduced cell viability to 28 ±6% when compared to the untreated control (n=4, p36 hours fluorescence was measured at excitation 488 nm and emission 527 nm (e.g., DCFDA kit). We found that methylglyoxal (1200 µM) significantly increased ROS by 205±25% when compared to the untreated control baseline (n=4, p
Embargo Period
5-24-2019
The Effects of Metformin, Aminoguanidine, and Pyridoxamine on Methylglyoxal Induced Cardiac Myocyte Injury
Philadelphia, PA
Advanced glycation end (AGE) products have been under investigation for their role in cardiovascular disease in complications. Methylglyoxal, a byproduct of glucose metabolism, is elevated in the blood of diabetic patients and has shown to be an important intermediate in the production of AGEs. Due to the highly reactive structure of methylglyoxal, it can produce high levels of reactive oxygen species (ROS) within the cell via mitochondrial modification which results in a loss of cell membrane potential and possible cell death. The role of methylglyoxal in cardiac cells is not well known; in this study methylglyoxal induced cell injury and ROS generation were investigated by co-treatment of methylglyoxal with metformin, aminoguanidine hydrochloride, or pyridoxamine dihydrochloride. The effects of methylglyoxal on H9C2 myoblast viability were evaluated after incubation of drugs for 24 hours by measuring absorbance at 450 nm by using tetrazolium to differentiate metabolically active and inactive cells (e.g., CCK-8 kit). We found that methylglyoxal (1200 µM) significantly reduced cell viability to 28 ±6% when compared to the untreated control (n=4, p36 hours fluorescence was measured at excitation 488 nm and emission 527 nm (e.g., DCFDA kit). We found that methylglyoxal (1200 µM) significantly increased ROS by 205±25% when compared to the untreated control baseline (n=4, p
Comments
Presented at Experimental Biology 2019.