To investigate whether microRNA‐24 (miR‐24) targeting C‐myc affects chondrocytes of rats with osteoarthritis (OA) via the MAPK signaling pathway. Thirty rats were assigned as a sham group and an OA group (established as OA rat models by cutting the anterior cruciate ligaments and removing 1/3 medial meniscus). TUNEL staining and immunohistochemistry were conducted for cell apoptosis index (AI) and positive expression rate of C‐myc protein. Enzyme‐linked immuno sorbent assay (ELISA) was carried out for serum level of IL‐1β and TNF‐α. Primary chondrocytes were assigned into the blank, negative control (NC), miR‐24 mimics, miR‐24 inhibitors, siRNA‐C‐myc, and miR‐24 inhibitors+siRNA‐C‐myc groups. The expressions of miR‐24, C‐myc, p38, ERK, JNK, IL‐1β, and TNF‐α in tissues and cells were detected using reverse transcription quantitative real‐time polymerase chain reaction (RT‐qPCR) and Western blotting. CCK8 assay and flow cytometry were performed for cell proliferation and apoptosis. The OA group showed higher IL‐1β, TNF‐α, AI, and C‐myc than the sham group. C‐myc is a target gene of miR‐24. Compared with the blank group, the miR‐24 mimics and siRNA‐C‐myc groups showed reduced expression of C‐myc, IL‐1β, TNF‐α, p38, p‐p38, ERK, p‐ERK, JNK, and p‐JNK, apoptosis rate yet increased cell proliferation; however, the miR‐24 inhibitors group exhibited an opposite trend. The miR‐24 inhibitors+siRNA‐C‐myc group presented a same tendency compared to the siRNA‐C‐myc group. Upregulated miR‐24 downregulates C‐myc could suppress apoptosis and promote proliferation of chondrocytes to prevent the occurrence and subsequent progression of OA via inactivating the MAPK signaling pathway.