Emodin alleviates mechanical stress-induced chondrocyte apoptosis via the Piezo1 channel

This study investigates the protective effects of emodin on mechanical stress-induced chondrocyte apoptosis, focusing on the role of the Piezo1 channel.Rabbit articular chondrocytes were subjected to varying levels of mechanical stress, and the impact of emodin was evaluated using apoptosis assays, calcium measurements, Western blot analysis, and Reverse transcription-quantitative polymerase chain reaction.Under high mechanical strain, Piezo1 expression and intracellular calcium levels significantly increased, correlating with elevated apoptosis.Emodin treatment downregulated Piezo1 expression, decreased calcium influx, and reduced apoptosis rates.To clarify the involvement of Piezo1, we used gene silencing and pharmacological activation strategies.Piezo1 knockdown enhanced the protective effects of emodin, whereas its activation diminished them, resulting in increased apoptosis.These findings indicate that the therapeutic effects of emodin may be mediated by its ability to inhibit Piezo1 activity, thereby offering a potential multi-targeted approach for conditions like osteoarthritis, where excessive mechanical stress accelerates joint degeneration.The modulation of Piezo1 and calcium signaling by emodin presents a novel intervention for mechanical stress-related joint diseases.