Abstract. Wogonoside possesses anti-oxidative, anti-inflammatory, anti-allergy and anti-tumor properties. The aim of the present study was to evaluate whether wogonoside alleviates spinal cord injury (SCI)-induced inflammation via nuclear factor (NF)-κB and nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome activation. Sprague-Dawley rats were positioned in the jaws of a calibrated aneurysm clip with a closing pressure of 55 g. The jaws were placed on the dorsal and ventral surfaces of the spinal cord and left in place for 1 min. SCI rats were treated with 12, 25 and 50 mg/kg wogonoside. Following this, the locomotor function was assessed using the Basso Beattie Bresnahan scale. The water content of the spinal cord was measured, tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 levels were assessed and western blot analysis was performed to evaluate the expressions of NF-κB and NLRP3. Wogonoside was demonstrated to significantly ameliorate the SCI-induced reduction in Basso Beattie Bresnahan score (P<0.01) and significantly reduce the water content of the spinal cord in rats with SCI-induced inflammation (P<0.01). Results also indicated that treatment with wogonoside significantly reduced the levels of IL-1β, TNF-α and IL-6 in rats with SCI-induced inflammation (P<0.01), potentially via the phosphorylation of NF-κB inhibitor α. Furthermore, treatment with wogonoside inhibited the expressions of toll-like receptor 4, NLRP3 and caspase-1 protein in SCI model rats (P<0.01). In conclusion, the results of the present study suggest that wogonoside alleviates SCI-induced inflammation by suppressing NF-κB and NLRP3 inflammasome activation.

Osteosarcoma (OS) is the most frequent primary bone malignancy and affects adolescents and young adults. Recently dysregulation of miRNAs has received more attention because of its extensive role in OS carcinogenesis. This research was designed to verify how microRNA-93 (miR-93) and tissue inhibitor of matrix metalloproteinase 2 (TIMP2) be involved in OS development. At first, the levels of miR-93 and its predictive target gene TIMP2 were detected in OS and osteoblast cell lines, and 62 pairs OS and adjacent non-OS specimens by real-time PCR and western blot. Then, viability, invasion, and epithelial mesenchymal transition (EMT) of OS cell lines were examined when overexpressed or knocked down miR-93, or overexpressed TIMP2. Finally, the interaction between miR-93 and TIMP2 was evaluated using mutation, gain, and loss experiment. Our data indicated that miR-93 was increased while TIMP2 was decreased in both OS cell lines and tissues. MiR-93 high-expression and TIMP2 low-expression were related with poor overall survival and prognosis of OS patients. Overexpression or knockdown experiment indicated that miR-93 enhanced OS cell viability, invasion, and EMT expression. TIMP2 could inhibit OS cell viability, invasion, and EMT expression. Further, miR-93 directly targeted TIMP2 and negatively regulated TIMP2 level in OS cells. And up-regulation of TIMP2 reversed the effects of miR-93 in OS. Finally, miR-93 regulated the oncogenic functions in OS cells by regulating the expression of TIMP2. In conclusion, our study demonstrates that miR-93 may exert an oncogenic function while TIMP2 may act as a tumor suppressor on OS.

CCAL1, a member of the tumor necrosis factor receptor superfamily 11B, encodes osteoprotegerin. We report that CCAL1 is highly expressed in osteoarthritis (OA) tissues and Human Chondrocyte‐Osteoarthritis (HC‐OA) cells and its expression level is positively correlated with the severity of OA. CCAL1 could activate NF‐κB and inhibit AMPK pathways to promote HC‐OA cell fibrosis, viability and proliferation.