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.

中文翻译：

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帕瑞昔布钠对缺血再灌注所致肠损伤的保护作用。

缺血再灌注 (I/R) 诱导的肠道损伤是导致氧化应激和炎症反应的病理生理过程，揭示其潜在机制对于制定治疗策略至关重要。据报道，环氧合酶 (COX) 与 I/R 损伤有关。帕瑞昔布钠是一种 COX-2 选择性抑制剂，具有保护作用，例如减少 I/R 引起的心脏、肾脏和大脑损伤。然而，帕瑞昔布钠在保护小肠免受 I/R 损伤方面的潜在作用却很少被研究。因此，本研究的目的是阐明帕瑞昔布钠在 I/R 诱导的肠损伤中的作用和潜在机制。总共将 60 只 Sprague-Dawley 大鼠随机分为四组：对照组（假手术）组、肠道 I/R 组、10 mg/kg 帕瑞昔布钠预处理 I/R (I/R + Pare/10) 组和 20 mg/kg 帕瑞昔布钠预处理 I/R (I/R + Pare /20) 组。建立常规I/R模型诱导大鼠肠道损伤。在缺血前连续 5 天每天一次将 10 或 20 mg/kg 的帕瑞昔布钠给予 I/R + Pare 组的大鼠腹膜内给药。再灌注后2小时采集血样和小肠组织。使用ELISA测定丙二醛、一氧化氮、白细胞介素（IL）-1β、IL-8、细胞间细胞粘附分子-1和IL-10水平的变化，以及总抗氧化能力的变化，以及超氧化物酶的活性歧化酶和髓过氧化物酶。此外，总 caspase-3、cleaved caspase-3、通过蛋白质印迹分析检查 Bcl-2 和 Bax。此外，检查再灌注后 7 天的每日存活率。结果表明，帕瑞昔布钠增加了抗氧化剂的水平并抑制了 I/R 诱导的肠道氧化损伤。此外，帕瑞昔布钠下调促炎因子的表达水平，但上调抗炎因子的表达水平。结果还表明，帕瑞昔布钠可减轻 I/R 诱导的细胞凋亡并提高大鼠的存活率。因此，在肠道 I/R 之前给予帕瑞昔布钠可通过抑制 I/R 诱导的炎症、氧化应激和细胞凋亡来减轻肠道损伤并提高大鼠存活率。检查再灌注后7天的每日存活率。结果表明，帕瑞昔布钠增加了抗氧化剂的水平并抑制了 I/R 诱导的肠道氧化损伤。此外，帕瑞昔布钠下调促炎因子的表达水平，但上调抗炎因子的表达水平。结果还表明，帕瑞昔布钠可减轻 I/R 诱导的细胞凋亡并提高大鼠的存活率。因此，在肠道 I/R 之前给予帕瑞昔布钠可通过抑制 I/R 诱导的炎症、氧化应激和细胞凋亡来减轻肠道损伤并提高大鼠存活率。检查再灌注后7天的每日存活率。结果表明，帕瑞昔布钠增加了抗氧化剂的水平并抑制了 I/R 诱导的肠道氧化损伤。此外，帕瑞昔布钠下调促炎因子的表达水平，但上调抗炎因子的表达水平。结果还表明，帕瑞昔布钠可减轻 I/R 诱导的细胞凋亡并提高大鼠的存活率。因此，在肠道 I/R 之前给予帕瑞昔布钠可通过抑制 I/R 诱导的炎症、氧化应激和细胞凋亡来减轻肠道损伤并提高大鼠存活率。帕瑞昔布钠下调促炎因子的表达水平，但上调抗炎因子的表达水平。结果还表明，帕瑞昔布钠可减轻 I/R 诱导的细胞凋亡并提高大鼠的存活率。因此，在肠道 I/R 之前给予帕瑞昔布钠可通过抑制 I/R 诱导的炎症、氧化应激和细胞凋亡来减轻肠道损伤并提高大鼠存活率。帕瑞昔布钠下调促炎因子的表达水平，但上调抗炎因子的表达水平。结果还表明，帕瑞昔布钠可减轻 I/R 诱导的细胞凋亡并提高大鼠的存活率。因此，在肠道 I/R 之前给予帕瑞昔布钠可通过抑制 I/R 诱导的炎症、氧化应激和细胞凋亡来减轻肠道损伤并提高大鼠存活率。