We have previously reported that intra-articular injection of xanthan gum (XG) could significantly ameliorate the degree of joint cartilage degradation and pain in experimental osteoarthritis (OA) model in vivo. In this present study, we evaluated the protective effect of XG against Sodium nitroprusside (SNP)-induced rabbit articular chondrocytes apoptosis in vitro. Rabbit articular chondrocytes were incubated with various concentrations of XG for 24h prior to 0.5mmol/L SNP co-treatment for 24h. The proliferation of chondrocytes was analyzed using MTT assay. The chondrocytes early apoptosis rates were evaluated using Annexin V-FITC/PI flow cytometry. The morphology of apoptosis chondrocytes were observed by scanning electron microscopy (SEM). The loss/disruption of mitochondrial membrane potential was detected using rhodamin 123 by confocal microscope. The concentration of prostaglandin E2 (PGE2) in cell culture supernatants was evaluated using ELISA assay. The results showed that XG could significantly reverse SNP-reduced cell proliferation and inhibited cell early apoptosis rate in a dose-dependent manner. XG alleviated loss/disruption of mitochondrial membrane potential and decreased the PGE2 level of chondrocytes cell culture supernatants in SNP-induced chondrocytes. These results of the present research strongly suggest that XG can protect rabbit articular chondrocytes against SNP-induced apoptosis in vitro.
Keywords: 3,5-Diphenyl-1-(4,5-dimethyl-2-thiazolyl) formazan (PubChem CID: 3634887); Apoptosis; Nitroprusside (PubChem CID: 11963622); Propidium iodide (PubChem CID: 104981); Rabbit chondrocytes; Rhodamin 123 (PubChem CID: 9929799); Sodium hyaluronate (PubChem CID: 3084049); Sodium nitroprusside; Xanthan gum; Xanthan gum (PubChem CID: 7107).
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