Quercetin prevents the loss of chondrogenic capacity in expansion cultured human auricular chondrocytes by alleviating mitochondrial dysfunction

The results reveal that quercetin attenuates chondrocyte senescence by alleviating mitochondrial dysfunction, thereby preventing the loss of chondrogenic function in chondrocytes subjected to long-term expansion culture.

Auricular chondrocytes exhibited senescence-related characteristics after prolonged expansion in culture. To identify senescence inducers, transcriptome sequencing was performed, with findings corroborated by transmission electron microscopy analyses. Quercetin was employed as an intervention to mitigate cellular senescence progression. The alterations in cellular senescence and mitochondrial function were evaluated. Regenerative cartilage tissue was developed through in vitro chondrogenic induction and in vivo implantation with GelMA hydrogel-loaded cells in nude mice. The impact of quercetin was substantiated through histological examinations.

To explore the characteristics of cellular senescence in human auricular chondrocytes during long-term in vitro culture and to evaluate the effects of anti-senescence treatments on enhancing their chondrogenic function.

Mitochondrial dysfunction was a key characteristic of auricular chondrocytes after long-term expansion culture. Chondrocytes cultured with quercetin showed a lower proportion of senescent cells and reduced mitochondrial dysfunction. The chondrocytes cultured with continuous application of quercetin formed higher quality regenerative cartilage both in vitro and in vivo compared to the control group.