ABSTRACT
We sequenced the complete mitochondrial genome of the copepod Labidocera rotunda (family Pontellidae) collected from Ihotaewoo Beach in Jeju, Korea. The mitochondrial genome was 16,564 bp in length and contained 13 protein-coding genes (PCGs), 22 transfer RNAs, and two ribosomal RNAs. The concatenated phylogenetic tree of L. rotunda was reconstructed using the maximum-likelihood method based on the eight PCGs obtained from eight species of copepods including L. rotunda. The results of the phylogeny analysis showed that L. rotunda was closely related to the family Temoridae among the three families. The complete mitochondrial genome of L. rotunda analyzed for the first time in this study provides insight into the phylogenetic and evolutionary relationship of Labidocera.
ABSTRACT
Schisandrol A possesses pharmacological properties and is used to treat various diseases; however, its effects on osteoarthritis (OA) progression remain unclear. Here, we investigated Schisandrol A as a potential therapeutic agent for OA. In vitro, Schisandrol A effects were confirmed based on the levels of expression of catabolic factors (MMPs, ADAMTS5, and Cox2) induced by IL-1ß or Schisandrol A treatment in chondrocytes. In vivo, experimental OA in mice was induced using a destabilized medial meniscus (DMM) surgical model or oral gavage of Schisandrol A in a dose-dependent manner, and demonstrated using histological analysis. In vitro and in vivo analyses demonstrated that Schisandrol A inhibition attenuated osteoarthritic cartilage destruction via the regulation of Mmp3, Mmp13, Adamts5, and Cox2 expression. In the NF-κB signaling pathway, Schisandrol A suppressed the degradation of IκB and the phosphorylation of p65 induced by IL-1ß. Overall, and Schisandrol A reduced the expression of catabolic factors by blocking NF-κB signaling and prevented cartilage destruction. Therefore, Schisandrol A attenuated OA progression, and can be used to develop novel OA drug therapies.
