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.