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Osteoarthritis (OA) is a multifactorial and chronic disease describing the destruction of cartilage that can lead to defects in the elderly. There is currently no practical strategy that can reverse the OA process. Here, we describe nepetin, a small natural compound with extracellular matrix (ECM) and inflammation regulating functions. In this study, we investigated the therapeutic effects of nepetin on interleukin‐1β (IL‐1β)‐induced inflammation in mice chondrocyte and OA model. In chondrocytes, treatment with nepetin inhibited the overexpression of pro‐inflammatory cytokines and mediators induced by IL‐1β. Moreover, pretreatment or posttreatment with nepetin also reduced the ECM catabolism and enhanced the ECM anabolism. Mechanistically, nepetin suppressed NF‐κB signaling pathway in IL‐1β stimulated chondrocyte. Meanwhile, our molecular docking studies indicated nepetin had a powerful binding capacity to p65. Furthermore, nepetin showed a protective and therapeutic effect on the mouse OA model. To sum up, this study indicated nepetin had a new potential therapeutic option in OA. [ABSTRACT FROM AUTHOR]

Osteoarthritis (OA) is a degenerative joint disease characterized by destruction of articular cartilage. The inflammatory response is the most important factor affecting the disease process. As interleukin‐1β (IL‐1β) stimulates several key mediators in the inflammatory response, it plays a major role in the pathogenesis of OA. Maslinic acid (MA) is a natural compound distributed in olive fruit. Previous studies have found that maslinic acid has an inhibitory effect on inflammation, but its specific role in the progression of OA disease has not been studied so far. In this study, we aim to assess the protective effect of MA on OA progression by in vitro and in vivo experiments. Our results indicate that, in IL‐1β‐induced inflammatory response, MA is effective in attenuating some major inflammatory mediators such as nitric oxide (NO) and prostaglandin E2, and inhibits the expression of IL‐6, inducible nitric oxide synthase, cyclooxygenase‐2, and tumor necrosis factor‐α (TNF‐α) in a concentration‐dependent manner. Also, MA downregulated the expression levels of thrombospondin motif 5 (ADAMTS5) and matrix metalloproteinase 13 in chondrocytes, resulting in reduced degradation of its extracellular matrix. Mechanistically, MA exhibits an anti‐inflammatory effect by inactivating the PI3K/AKT/NF‐κB pathway. In vivo, the protective effect of MA on OA development can be detected in a surgically induced mouse OA model. In summary, these findings suggest that MA can be used as a safe and effective potential OA therapeutic strategy. [ABSTRACT FROM AUTHOR]

Objective: The aim of this meta‐analysis was to systematically evaluate the efficacy of augmentative plating (AP) and exchange nailing (EN) in the treatment of nonunion of femoral shaft fracture. Methods: For the present meta‐analysis, PubMed, EMBASE, and the Cochrane Library were searched to identify relevant articles up to April 2019. Two investigators independently evaluated the quality of original publications following the guidelines proposed by the Cochrane Handbook. Data were extracted from the studies and analyzed using Review Manager 5.3. Results: Five studies were included in this meta‐analysis, with a total of 506 patients. There were 232 patients in the AP group and 276 patients in the EN group. The AP group was associated with higher union rate (OR, 11.66; 95% CI, 4.31–31.50; P < 0.01), shorter union time (SMD, −1.10; 95% CI, −2.09 to −0.11; P = 0.03), shorter operation time (SMD, −0.55; 95% CI, −0.88 to −0.21; P < 0.01), less blood loss (SMD, −1.72; 95% CI, −3.33 to −0.11; P < 0.01), and fewer complications (OR, −0.11; 95% CI, −0.16 to −0.07; P < 0.01) than the EN group. Conclusion: The results of the meta‐analysis showed that AP is found to be superior for nonunion of femoral shaft fractures in both intraoperatively (ie, shorter operation time and less blood loss) and postoperatively (ie, higher union rate, shorter union time, and lower complication rate). Overall, AP was superior to EN in the treatment of nonunion of femoral shaft fractures after intramedullary nailing (IMN). [ABSTRACT FROM AUTHOR]

• Hederacoside-C inhibited the AGEs-induced inflammatory response in mice chondrocytes. • Hederacoside-C inhibited the AGEs-induced ECM degradation in mice chondrocytes. • Hederacoside-C inhibited AGEs-induced ECM degradation through suppressing NF-κB activation. Hederacoside-C (HDC), a natural compound extracted from the leaves of Hedera helix with inflammation modulatory properties in variety of disorders. In this study, we investigated the latent mechanism of HDC in alleviating of the progress of OA in vitro experiment. The results showed that HDC pretreatment suppressed the advanced glycation end-products (AGEs) induced over-regulation of ROS level and inflammatory factors. Moreover, HDC also downregulate the degradation of ECM induced by AGEs. Mechanistically, the HDC suppressed NF-κB signaling pathway in chondrocyte. To sum up, this study indicated HDC possessed a new potential therapeutic option in osteoarthritis. [ABSTRACT FROM AUTHOR]