Tendinopathy is an aging-related disease, often caused by micro-scarring and degeneration due to overuse or trauma. Ascorbic acid (vitamin C) supplementation is reported to be a useful treatment for tendinopathy recovery. We compared the inhibitory effects of various ascorbic acid doses on tendon cell damage. H2O2 was added to human-derived tendon cells in vitro (Group H2O2, control), followed by incubation with 150 µM or 30 mM of ascorbic acid (Group C, Group HC). The oxidative injury degree was evaluated by determining reactive oxygen species levels. The cytoskeletal structure was examined via fluorescence immunostaining of actin filaments. Quantitative polymerase chain reaction (qPCR) was performed to analyze the expressions of mitochondria transcription factor A, adenosine triphosphate 5A, type I collagen, and p16. Cell death was reduced, and oxidative stress was inhibited in C and HC groups. The cytoskeleton was maintained in the HC group but not in the C group. qPCR analysis revealed that p16 expression was inhibited in both the C and HC groups compared to the H2O2 group; other markers had increased expression. The progression of cell death and cytoskeletal disruption was inhibited by the administration of high-dose vitamin C. Hence, high-dose vitamin C is a potential treatment for tendon cell degeneration.
Keywords: actin filament; cellular senescence; high-dose vitamin C; mitochondrial damage; oxidative injury; tendon cell degeneration.