Icariin protects H9c2 cardiomyocytes from lipopolysaccharide‑induced injury via inhibition of the reactive oxygen species‑dependent c‑Jun N‑terminal kinases/nuclear factor-κB pathway.

The inflammatory response is involved in the pathogenesis of the most common forms of heart disease. Icariin has a number of pharmacological actions, including anti‑inflammatory, anti‑oxidative and anti‑apoptotic effects. However, the role of icariin in cardiac inflammation has remained elusive. In the present study, H9c2 rat cardiomyocytes were stimulated by lipopolysaccharide (LPS) and treated with icariin. The results showed that icariin significantly reduced the increase in the mRNA expression of tumor necrosis factor α, interleukin (IL)‑1β and IL‑6 that occurred in response to LPS. Furthermore, icariin regulated the expression of B-cell lymphoma 2 and B-cell lymphoma 2-associated X, and rescued H9c2 cells from apoptosis. Incubation with 2',7'‑dichlorofluorescein diacetate demonstrated that icariin inhibited the production of intracellular reactive oxygen species (ROS). In addition, the phosphorylation of c‑Jun N‑terminal kinases (JNK), the degradation of inhibitor of κB and the nuclear translocation of nuclear factor‑κB (NF‑κB) p65 in LPS‑treated H9c2 cells were blocked by icariin treatment. These results suggested that icariin prevented cardiomyocytes from inflammatory response and apoptosis, and that this effect may be mediated by inhibition of the ROS‑dependent JNK/NF‑κB pathway.