We previously reported that treatment with chondroitin sulfate from sturgeon bone (CSSB) promoted anti-apoptotic activity in hydrogen peroxide (H2O2)-treated chondrocytes and had a protective effect on mitochondria. It is known that cells can repair damaged mitochondria through autophagy, thus inhibiting the development of apoptosis. Therefore, it is reasonable to speculate that CSSB treatment may inhibit chondrocyte apoptosis via regulation of autophagy. We observed the mitochondrial morphology of chondrocytes treated with different doses of CSSB, and confirmed that CSSB did not affect cell activity or cause damage to mitochondria. When compared with H2O2 treatment alone, CSSB treatment increased the clearance and repair of damaged mitochondria and promoted fusion of damaged mitochondria and lysosomes. CSSB treatment also increased the number of autolysosomes. However, these events could be blocked in chondrocytes pretreated with the autophagy inhibitor chloroquine, resulting in a decreased level of autophagy and increased apoptosis. These results suggest that CSSB treatment helps maintain intracellular homeostasis and prevent injury in chondrocytes treated with H2O2 by increasing autophagy.
Keywords: Autophagy; Chondrocyte damage; Chondroitin sulfate; Hydrogen peroxide; Sturgeon bone.
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