High glucose induces myocardial cell injury through increasing reactive oxygen species production

• Published in: Asian Pacific Journal of Tropical Medicine
• Main Authors: Yu-Jun Wang, Xiao-Yu Lyu, Li Yu
• Format: Article in Journal/Newspaper
• Language: English
• Published: Wolters Kluwer Medknow Publications 2018
• Subjects: diabetic cardiomyopathy; high glucose; myocardial cells; reactive oxygen species; apoptosis; collagen; Arctic medicine. Tropical medicine; RC955-962; Arctic
• Online Access: https://doi.org/10.4103/1995-7645.223575; https://doaj.org/article/188b08266312409593050fb1cbe1a04d

Objective: To study the injury effect and molecular mechanism of high glucose on myocardial cells. Methods: Myocardial cells H9c2 were cultured and divided into the control group treated with DMEM containing 5.5 mmol/L glucose, the high glucose group treated with DMEM containing 35 mmol/L glucose, and the N-acetylcysteine (NAC) group pre-treated with 1 000 μmol/L NAC and treated with DMEM containing 1 000 μmol/L NAC and 35 mmol/L glucose. The production of ROS and the expression of mitochondria pathway apoptosis molecules in cells as well as the contents of collagen and collagen metabolism molecules were measured. Results: After 8 h, 16 h and 24 h of treatment, ROS RFU as well as Bax, CytC, Caspase-3 and Caspase-9 protein expression in cells and Col-I, Col-III, PINP and PIIINP protein levels in culture medium of high glucose group were higher than those of control group, Bcl-2 protein expression were lower than those of control group, but CTX-I protein levels in culture medium were not significantly different from those of control group; after 24 h of treatment, Bax, CytC, Caspase-3 and Caspase-9 protein expression in cells as well as Col-I, Col-III, PINP and PIIINP protein levels in culture medium of NAC group were lower than those of high glucose group whereas Bcl-2 protein expression was higher than that of high glucose group. Conclusions: High glucose can induce myocardial cell apoptosis, increase collagen synthesis and accelerate interstitial fibrosis by increasing the production of reactive oxygen species.