Electroacupuncture inhibits sodium nitroprusside‑mediated chondrocyte apoptosis through the mitochondrial pathway

In China, electroacupuncture (EA) is a therapeutic method that is extensively applied in the clinical treatment of osteoarthritis (OA); however, the underlying molecular mechanism remains unclear. Chondrocyte apoptosis may be observed in cartilage tissue in OA, and is often considered a key target for the treatment of this condition. Therefore, the present study aimed to determine the effects of EA on sodium nitroprusside (SNP)‑induced chondrocyte apoptosis. Chondrocytes were obtained from the knee joints of Sprague Dawley rats by type II collagenase digestion. Following microscopic observation and authentication with type II collagen immunohistochemistry, articular cartilage cells were used in subsequent experiments. Using inverted phase contrast microscopy, DAPI staining and flow cytometry, it was revealed that chondrocytes treated with SNP became apoptotic, whereas EA inhibited SNP‑induced chondrocyte apoptosis. Subsequently, JC‑1 single staining, reverse transcription‑quantitative polymerase chain reaction analysis, western blotting, colorimetric assays and immunofluorescence staining were performed for further investigation. The results demonstrated that, when compared with normal chondrocytes, the mitochondrial membrane potential of SNP‑treated chondrocytes was markedly lowered, B‑cell lymphoma 2 (Bcl‑2) expression was reduced, and the expression levels of Bcl‑2‑associated X protein (Bax), cytochrome c, caspase‑9 and caspase‑3 were increased. Compared with in SNP‑treated chondrocytes, the decrease in the mitochondrial membrane potential of chondrocytes treated with SNP and EA was smaller, Bcl‑2 expression was increased, and the expression levels of Bax, cytochrome c, caspase‑9 and caspase‑3 were decreased following EA intervention. In conclusion, the present study demonstrated that EA modulated the mitochondrial pathway to suppress SNP‑mediated chondrocyte apoptosis. Therefore, EA may be of value in the treatment of OA.