Objective To explore the specific mechanism of O3 acting on osteoarthritis (OA) by observing the expression of Notch signaling pathway-related factors (Notch-1, Jagged1, keratin1, involucrin) and apoptosis biomarkers (caspase-3, Bax, Bcl-2) in rat OA chondrocytes.Methods Twenty-four SD rats were selected and divided into blank group, model group and model+O3 treatment group randomly(8 rats in each group) before the reproduction of OA model (right knee) by intraarticular injection of papain-cysteine mixture. Every week after the successful modeling, 2 mL of O3 (25 μg/mL) was injected into the right knee joint cavity of the rats in the model+O3 treatment group, the model group was injected with an equal volume of air, and the blank group was not treated. After 4 weeks of treatment, the rats were sacrificed and the knee OA articular cartilage tissue was collected and observed by HE staining. The expression of caspase-3 and Notch-1 was detected by immunofluorescence and the expression of Notch-1, Jagged1, Bcl-2, keratin1, and keratin1 were detected by Western Blot.Results HE staining revealed that the model+O3 treatment group could effectively change the cartilage degeneration, make the chondrocytes proliferate in clusters and the tide line interrupted. Immunohistochemistry and Western Blot detection showed that, compared with the blank group, caspase-3, Notch-1, Jagged1 and the protein contents of Bax were significantly increased in the model group (P<0.05). Compared with the model group, the contents of the above proteins were decreased in the model+O3 treatment group, among which caspase-3 and the protein contents of Notch-1 decreased more substantially compared with the model group, which means the difference was statistically significant (P<0.05); Bcl-2, keratin1 and the protein contents of involucrin were greatly decreased in the model group (P<0.05), and the above protein contents were dramatically increased after O3 treatment (P<0.05).Conclusion The Notch signaling pathway participates in the development of OA by regulating the apoptosis of OA chondrocytes while O3 can reduce chondrocyte apoptosis by inhibiting the Notch signaling pathway and consequently protect articular cartilage, and delay the progression of OA. |