Abstract
Ischemia reperfusion (I/R)‑induced intestinal injury is a pathophysiological 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 intraperitoneally 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 molecule‑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 analysis. 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.