The aim of the present study was to investigate the protective effect of cytokine response modifier A (CrmA) released from chitosan (CS) microspheres in a controlled manner on interleukin (IL)‑1β‑induced inflammation and apoptosis in chondrocytes. The CrmA release kinetics were characterized by an initial burst release, which was reduced to a linear release over 8 days. Furthermore, chondrocytes were isolated from 1‑week‑old Sprague Dawley rats. The cell culture was established by stimulation with 10 ng/ml IL‑1β and subsequent incubation with CS‑CrmA microspheres. Following stimulation with IL‑1β, the viability of chondrocytes was decreased. However, the cell viability was attenuated by CS‑CrmA microspheres as revealed by a cell counting kit‑8 assay. CS‑CrmA microspheres significantly inhibited IL‑1β‑induced inflammation in chondrocytes by attenuating increases in the gene expression levels of inducible nitric oxide synthase and cyclooxygenase‑2, as well as the concentrations of nitric oxide and prostaglandin E2. CS‑CrmA microspheres significantly decreased the number of apoptotic chondrocytes induced by IL‑1β as indicated by a terminal deoxyribonucleotide transferase deoxyuridine triphosphate nick‑end labeling assay. In addition, CS‑CrmA microspheres blocked IL‑1β‑induced chondrocyte apoptosis by increasing B‑cell lymphoma 2 (Bcl‑2) and decreasing Bcl‑2‑associated X protein, caspase‑3 and poly adenosine diphosphate‑ribose polymerase expression at the mRNA and protein levels, as indicated by reverse‑transcription quantitative polymerase chain reaction and western blot analysis, respectively. The results of the present study revealed that CS‑CrmA microspheres, as a controlled release system of CrmA, may protect rat chondrocytes from IL‑1β‑induced inflammation and apoptosis via regulating inflammatory and apoptosis‑associated genes.

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