Amygdalin attenuates interleukin-1β-stimulated chondrocyte damage in mice through the Nrf2/NF-κB pathway

Osteoarthritis (OA) is the most usual joint disease, which affects the life of patients and causes them seriously physical pain. Amygdalin, the main active pharmaceutical ingredient in Semen Armeniacae Amarum, has anti-inflammatory, anti-oxidation, and immunomodulatory impacts. However, the regulatory functions of Amygdalin in OA progression keep indistinct and need further investigations. This study is aimed to probe the regulatory influences and associated pathways of Amygdalin in OA development.

The cell viability was confirmed through CCK-8 assay. The levels of PGE2, TNF-α and IL-6 were detected through ELISA. The ROS level was examined through DCF staining. The levels of MDA, SOD and GSH were measured through the commercial kit. The protein expressions were evaluated through western blot.

Firstly, it was demonstrated that Amygdalin can refrain IL-1β-evoked inflammation in chondrocytes. Next, Amygdalin repressed IL-1β-triggered oxidative stress in chondrocytes. Moreover, Amygdalin inhibited IL-1β-mediated ECM degradation in chondrocytes. Lastly, it was revealed that Amygdalin accelerated the Nrf2 pathway and suppressed the NF-κB pathway.

Amygdalin attenuated IL-1β-stimulated chondrocyte damage through the Nrf2/NF-κB pathway, thereby ameliorating OA progression. This finding hinted that Amygdalin may be one promising drug for OA treatment.