Cardioprotective effect of 6-shogaol against hyperglycemia-induced toxicity in H9c2 cardiomyocytes via suppressing of NF-κB pathway.

Diabetic cardiomyopathy (DC) is a serious complication of diabetes. Apoptosis, inflammatory and ROS production are among the factors that are involved in the progression of diabetic cardiomyopathy. 6-shogaol is reported to inhibit apoptosis and reduce inflammatory and ROS production. This study aimed to study the effect of 6-shogaol (6S) on the progression of diabetic cardiomyopathy in vitro. To develop DC model, H9c2 cell line was exposed to high glucose (HG) level (33 M glucose) for 24 h and used as a model for diabetic cardiomyopathy. Another set of H9c2 cell lines were 1 h pretreated with different conc. of 6-shogaol (5-20 mu M). Cell viability, apoptosis, ROS production, IL-6, TNF-alpha and NF-kB were estimated in these cell lines treated with HG level or pretreated with 6-shgoal before HG. Exposing cardiomyocytes H9c2 cells to HG produced dramatic changes in cell biology and chemistry. There is a significant reduction in cell viability and enhancement in cell apoptosis as compared with control. In addition, ROS production, IL-6, TNF-alpha levels were increased in H9c2 line treated with HG Also, there is overexpression of NF-kappa B in cells treated with HG levels alone. On the other hand, pretreatment of cardiomyocytes H9c2 cells with 6-shogaol (5-20 mu M) significantly improved cell viability and reduced apoptosis, in addition, 6S at a dose of 10 mu M abrogated the deleterious effects of HG on oxidative stress and inflammatory parameters via modulation of NF-kappa B pathway. Therefore, 6S has a potential protective effect against hyperglycemia-induced DC in vitro.