Department of Burns and Cutaneous Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shannxi 710032, PR China.
Chem Biol Interact. 2013 Aug 25;204(3):166-72. doi: 10.1016/j.cbi.2013.05.010. Epub 2013 Jun 3.
Inflammation and oxidative stress exert important roles in intestinal ischemia-reperfusion injury (IRI). Lycium barbarum polysaccharides (LBPs) have shown effective antioxidative and immunomodulatory functions in different models. The purpose of the present study was to assess the effects and potential mechanisms of LBPs in intestinal IRI. Several free radical-generating and lipid peroxidation models were used to assess the antioxidant activities of LBPs in vitro. A common IRI model was used to induce intestinal injury by clamping and unclamping the superior mesenteric artery in rats. Changes in the malondialdehyde (MDA), tumor necrosis factor (TNF)-α, activated nuclear factor (NF)-κB, intracellular adhesion molecule (ICAM)-1, E-selectin, and related antioxidant enzyme levels, polymorphonuclear neutrophil (PMN) accumulation, intestinal permeability, and intestinal histology were examined. We found that LBPs exhibited marked inhibitory action against free radicals and lipid peroxidation in vitro. LBPs increased the levels of antioxidant enzymes and reduced intestinal oxidative injury in animal models of intestinal IRI. In addition, LBPs inhibited PMN accumulation and ICAM-1 expression and ameliorated changes in the TNF-α level, NF-κB activation, intestinal permeability, and histology. Our results indicate that LBPs treatment may protect against IRI-induced intestinal damage, possibly by inhibiting IRI-induced oxidative stress and inflammation.
炎症和氧化应激在肠缺血再灌注损伤（IRI）中发挥重要作用。枸杞多糖（LBPs）在不同模型中显示出有效的抗氧化和免疫调节功能。本研究旨在评估 LBPs 在肠 IRI 中的作用及其潜在机制。使用几种自由基生成和脂质过氧化模型来评估 LBPs 的体外抗氧化活性。使用常见的 IRI 模型通过夹闭和松开肠系膜上动脉在大鼠中诱导肠损伤。检测丙二醛（MDA）、肿瘤坏死因子（TNF）-α、激活核因子（NF）-κB、细胞间黏附分子（ICAM）-1、E-选择素和相关抗氧化酶水平、多形核中性粒细胞（PMN）聚集、肠通透性和肠组织学的变化。我们发现 LBPs 在体外对自由基和脂质过氧化具有明显的抑制作用。LBPs 增加了抗氧化酶的水平，并减轻了肠 IRI 动物模型中的肠氧化损伤。此外，LBPs 抑制了 PMN 聚集和 ICAM-1 表达，并改善了 TNF-α 水平、NF-κB 激活、肠通透性和组织学的变化。我们的结果表明，LBPs 治疗可能通过抑制 IRI 诱导的氧化应激和炎症来保护肠免受损伤。
