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丁酸钠减轻盲肠结扎穿刺诱导脓毒症大鼠肠道损伤并提高其生存率。

Sodium Butyrate Ameliorates Intestinal Injury and Improves Survival in a Rat Model of Cecal Ligation and Puncture-Induced Sepsis.

机构信息

Department of Critical Care Medicine, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Heping District, Shenyang, 110004, Liaoning Province, China.

出版信息

Inflammation. 2019 Aug;42(4):1276-1286. doi: 10.1007/s10753-019-00987-2.

Abstract

Sepsis is a life-threatening condition with a high rate of mortality. Unfortunately, very few therapies can improve outcomes in patients with sepsis. Butyrate, which is the most potent histone deacetylase (HDAC) inhibitor among short-chain fatty acids, exerts anti-inflammatory effects in a variety of inflammatory diseases. Butyrate might thus be valuable in the treatment of sepsis, in which inhibition of overwhelming cytokine release is vitally important. Sepsis was induced in 7- to 8-week-old Sprague-Dawley rats by cecal ligation and puncture (CLP) with a 21-g double-puncture technique. Rats received an intravenous injection of normal saline (vehicle) or sodium butyrate (200 mg/kg) after CLP and were sacrificed 12 h later. Hematoxylin and eosin staining was performed to observe the intestinal mucosal morphology. RT-PCR and ELISA were used to determine the intestinal inflammatory response in vivo. Intestinal permeability was evaluated by measuring fluorescein isothiocyanate dextran (FD-4) absorption in vivo, and tight junction protein expression was examined by western blot. NF-κB p65 activities were assessed by western blot and immunohistochemistry. Sodium butyrate treatment improved the survival rate of CLP rats and alleviated sepsis-induced intestinal mucosal injury. Proinflammatory cytokine expression was lower in butyrate-treated rats than in the vehicle group. FD-4 leakage from the intestinal tract was reduced, and the expression levels of the tight junction proteins claudin-1 and ZO-1 were also restored in rats that received sodium butyrate treatment. These effects were associated with less NF-κB p65 nuclear translocation, whereas the expression of Iκ-Bα was not affected or even increased. Sodium butyrate mitigates the inflammatory response and maintains intestinal barrier function in polymicrobial sepsis partly through inhibition of NF-κB activation and may serve as a novel therapy for sepsis.

摘要

脓毒症是一种危及生命的疾病,死亡率很高。不幸的是,很少有治疗方法可以改善脓毒症患者的预后。丁酸盐是短链脂肪酸中最有效的组蛋白去乙酰化酶 (HDAC) 抑制剂,在多种炎症性疾病中具有抗炎作用。因此,丁酸盐在治疗脓毒症方面可能具有价值,因为抑制过度的细胞因子释放至关重要。通过使用 21 号双穿刺技术进行盲肠结扎和穿刺 (CLP),在 7-8 周龄的 Sprague-Dawley 大鼠中诱导脓毒症。CLP 后,大鼠接受生理盐水(载体)或丁酸钠(200mg/kg)静脉注射,并在 12 小时后处死。进行苏木精和伊红染色以观察肠黏膜形态。RT-PCR 和 ELISA 用于体内测定肠炎症反应。通过测量荧光素异硫氰酸酯葡聚糖(FD-4)体内吸收来评估肠通透性,并通过 Western blot 检查紧密连接蛋白表达。通过 Western blot 和免疫组化评估 NF-κB p65 活性。丁酸钠治疗可提高 CLP 大鼠的存活率并减轻脓毒症引起的肠黏膜损伤。与载体组相比,丁酸钠处理大鼠的促炎细胞因子表达降低。丁酸钠治疗大鼠的 FD-4 从肠道漏出减少,紧密连接蛋白 claudin-1 和 ZO-1 的表达水平也得到恢复。这些作用与 NF-κB p65 核易位减少有关,而 Iκ-Bα 的表达不受影响甚至增加。丁酸钠通过抑制 NF-κB 激活减轻多微生物脓毒症中的炎症反应并维持肠屏障功能,可能是脓毒症的一种新疗法。

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