Carboxymethylated chitosan protects rat chondrocytes from NO‑induced apoptosis via inhibition of the p38/MAPK signaling pathway.

Abstract

In the present study, the effect of carboxymethylated chitosan (CMCS) on nitric oxide (NO)‑induced apoptosis, and activation of the p38/MAPK signaling pathway in chondrocytes were investigated. Cartilage was isolated from the knee joints of Sprague‑Dawley rats, and was used to establish cultured primary chondrocytes. The chondrocytes were incubated with the NO donor, sodium nitroprusside (SNP), to induce apoptosis, and were treated with CMCS and the p38 inhibitor, SB203580. Cell viability was assessed using a Cell Counting Kit‑8 assay. Apoptosis of the chondrocytes was detected using Annexin V‑fluorescein isothiocyanate/propidium iodide staining. The activation of p38 was detected using Western blot analysis, and caspase‑3 activity was detected using a caspase‑3 detection kit. The results indicated that, in chondrocytes treated with SNP, the optical density values of the experimental groups were significantly lower, compared with the control group (P<0.05). The exposure of the cells to CMCS significantly prevented apoptosis (P<0.05), and a dose‑dependent effect was demonstrated using fluorescence‑activated cell sorting analysis (P<0.05). Examination of the expression and activity of p38 and caspase‑3, respectively, showed that SNP increased the expression of p38 and activity of caspase‑3, and this trend was reversed following the addition of CMCS and SB203580. Taken together, these findings indicated that CMCS prevented NO‑induced apoptosis of chondrocytes via inhibition of the p38/mitogen‑activated protein kinase signaling pathway in vitro.