Sepsis caused by uncontrolled systemic inflammation is one of the leading causes of death around the world. Parecoxib is a selective COX-2-specific inhibitor which has been demonstrated to possess anti-inflammatory and antiseptic functions in an animal sepsis model. The present study was performed to examine the therapeutic efficacy of parecoxib against inflammation in a mouse model of cecal ligation and puncture (CLP). Male mice were randomly divided into Sham, Model (Sepsis), Dexmedetomidine (Dex), and Parecoxib groups, with 12 mice in each group. After surgery, parecoxib (0.1, 1 and 10 mg/kg) was intraperitoneally injected and survival rates were then measured. The levels of immunoglobulin and inflammatory factors in sera and spleen were measured by enzyme-linked immunosorbent assay (ELISA), Western blot and quantitative real-time polymerase chain reaction (qRT-PCR). Subtypes of lymphocyte subsets were detected by flow cytometry. Hematoxylin-eosin staining was performed to examine spleen injury. We discovered that parecoxib treatment improved survival rates in mice with sepsis, with the effect increasing with concentration. Compared with the model group, the amount of immunoglobulin was increased, inflammatory factor production was inhibited, proportions of T helper and regulatory T cells were reduced, pathological damage in mice spleen was ameliorated, COX-2 expression was inhibited, and phosphorylated-p65 (p-p65) was deactivated in the spleen of the mice treated with Dexmedetomidine (DEX) and Parecoxib. Our data suggest that Parecoxib inhibits the inflammatory response and has protective effects against sepsis in mice, and may have potential as a novel therapeutic method for treating sepsis.
This article is protected by copyright. All rights reserved.