Effect and mechanism of xanthan gum on osteoarthritis caused by anterior cruciate ligament transection / 药学学报

ABSTRACT

The study is designed to evaluate the protective effect of xanthan gum (XG) injection on cartilage injury in the rabbit osteoarthritis (OA) model induced by anterior cruciate ligament transection (ACLT), and to explore the effect of XG on the expression of caspase-3 and Bax protein in OA cartilage. Sixty male New Zealand white rabbits were randomly divided into 6 groups (n=10) according to random number table method, and one group was selected randomly as the normal control group (control) while the other 5 groups of right knee were used to establish the OA model with ACLT, which were then divided into model group (model), XG-0.6 mg·kg-1, XG-1.2 mg·kg-1, XG-2.4 mg·kg-1 treatment group and sodium hyaluronate (SH-1.2 mg·kg-1) treatment group according to drug intervention. The knee joint temperature and knee joint width of each group were measured in the course of treatment. After treatment, the macroscopic morphology of rabbit joints in each group was observed. The pathological morphology of articular cartilage of rabbits in each group was observed using HE staining. The expression of Bax and cleaved caspase-3 in the cartilage of rabbits were detected by Western blot. The result shows that XG inhibited the increase in knee joint temperature and knee width caused by OA in a dose-dependent manner. XG improved the morphological abnormalities and tissue injuries of the femoral condyle and tibial plateau caused by OA. Western blot result shows that, compared with the control group, the levels of Bax and cleaved caspase-3 in knee cartilage cells of model group and XG-0.6 mg·kg-1 group were significantly increased (P-1 group (P>0.05). These two groups are significantly higher than those of XG-1.2 mg·kg-1 and XG-2.4 mg·kg-1 (P-1 and XG-1.2 mg·kg-1 group (P>0.05). The level of Bax in knee cartilage in XG-2.4 mg·kg-1 group was lower than that of XG-1.2 mg·kg-1 group (P<0.05). In conclusion, XG effectively protected cartilage damage in OA, and inhibited the expression of Bax and caspase-3 protein in OA cartilage.