Li, Mei published the artcileProtective effect of parecoxib sodium against ischemia reperfusion-induced intestinal injury, COA of Formula: C19H17N2NaO4S, the publication is Molecular Medicine Reports (2021), 24(5), 776, database is CAplus and MEDLINE.
Ischemia reperfusion (I/R)-induced intestinal injury is a pathophysiol. process leading to oxidative stress and inflammatory responses, and revealing its underlying mechanisms is essential for developing therapeutic strategies. Cyclooxygenase (COX) has been reported to be involved in I/R injury. Parecoxib sodium, a selective inhibitor for COX-2, exerts protective effects, such as reducing I/R-induced injuries in the heart, kidney and brain. However, the potential role of parecoxib sodium in protecting the small intestine against I/R-induced injury has rarely been investigated. Therefore, the aim of the present study was to elucidate the effects and potential mechanisms of parecoxib sodium in I/R-induced intestinal injury. In total, 60 Sprague-Dawley rats were randomly divided into four groups: Control (sham operation) group, intestinal I/R group, 10 mg/kg parecoxib sodium-pre-treated I/R (I/R + Pare/10) group and the 20 mg/kg parecoxib sodium-pre-treated I/R (I/R + Pare/20) group. A regular I/R model was established to induce the intestinal injury in rats. Parecoxib sodium at 10 or 20 mg/kg was i.p. administered into rats in both I/R + Pare groups once daily for 5 consecutive days prior to ischemia. Blood samples and small intestinal tissues were collected at 2 h after reperfusion. Changes in the levels of malondialdehyde, nitric oxide, interleukin (IL)-1β, IL-8, intercellular cell adhesion mol.-1 and IL-10, as well as the total antioxidant capacity were determined using ELISA, as were the activities of superoxidase dismutase and myeloperoxidase. Furthermore, the protein expression levels of total caspase-3, cleaved caspase-3, Bcl-2 and Bax were examined via western blot anal. In addition, the daily survival rate post-reperfusion was examined for 7 days. It was revealed that parecoxib sodium increased the levels of antioxidants and suppressed the intestinal oxidative injury induced by I/R. Moreover, parecoxib sodium downregulated the expression levels of the proinflammatory factors, but upregulated the expression levels of anti-inflammatory factors. The results also demonstrated that parecoxib sodium attenuated I/R-induced apoptosis and increased the survival rate of rats. Thus, administration of parecoxib sodium prior to intestinal I/R attenuated intestinal injury and increased the rat survival rate by inhibiting I/R-induced inflammation, oxidative stress and apoptosis.
Molecular Medicine Reports published new progress about 198470-85-8. 198470-85-8 belongs to isoxazole, auxiliary class Immunology/Inflammation,COX, name is Sodium ((4-(5-methyl-3-phenylisoxazol-4-yl)phenyl)sulfonyl)(propionyl)amide, and the molecular formula is C19H17N2NaO4S, COA of Formula: C19H17N2NaO4S.
Referemce:
https://en.wikipedia.org/wiki/Isoxazole,
Isoxazole | C3H3NO – PubChem