6-Gingerol, an ingredient of Zingiber officinale, abrogates lipopolysaccharide-induced cardiomyocyte injury by reducing oxidative stress and inflammation

Background Sepsis-induced cardiac dysfunction is the main reason for the high mortality rate in patients with sepsis. For centuries, ginger has been used as a spice and a natural medicinal herb. Gingerols are phenolic compounds extracted from ginger that have promising pharmacological effects. The current research was designed to assess the effect of 6-gingerol on lipopolysaccharide-induced H9c2 cardiomyocyte injury and its underlying mechanisms. Methods H9c2 cells were pre-incubated for 24 h with a wide range of concentrations of 6-gingerol (5- 100 mu M). Afterward, 10 mu g/ml of LPS was added for another 24 h. Next, the cell viability, the level of reactive oxygen species (ROS) production, lipid peroxidation, and GSH content were measured using MTT, H2DCF-DA, TBA/TCA, and DTNB reagents. In addition, the levels of inflammatory mediators, i.e., interleukin (IL)-1 beta, tumor necrosis factor (TNF)-alpha, and IL-6, and their gene expression levels were evaluated using ELISA and quantitative real-time PCR. Results Our study revealed that LPS not only reduced cell viability, but also increased lipid peroxidation, ROS production, and cytokine levels, and decreased GSH levels. The concentration of 25, 50, and 100 mu M of 6-gingerol inhibited the LPS-induced H9c2 cellular injury via a decrement in the MDA (25 mu M: p< 0.05, 50 and 100 mu M: p< 0.001) and ROS production levels (25- 100 mu M: p< 0.001), while enhancing the GSH content (25- 100 mu M: p< 0.001). This phytochemical also attenuated the protein levels of TNF-alpha, IL-beta, and IL-6 (all: p< 0.001) and their related genes (all: p< 0.001) at concentrations of 50-100 mu M. Conclusion Pre-treatment with 6-gingerol has potential protective effects on LPS-injured cardiomyocytes by suppressing oxidative stress and inflammation.