To verify the above results that Sal B exerts its role in alleviating the development of arthritis via the miR-128-3p/SIRT1 axis, we overexpressed miR-128-3p or knocked down SIRT1 in ATDC5 cells followed by the treatment with PA and Sal B. MTT assay indicated that miR-128-3p overexpression or SIRT1 knockdown could weakened the effects of Sal B on cell viability in PA pretreating ATDC5 cells (Fig. 6B). The gene discussed is SIRT1; the disease is Arthritis.