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Evaluation of the effect of intraperitoneal etanercept administration on oxidative stress and inflammation indicators in the kidney and blood of experimental sepsis-induced rats

机译:腹膜内乙酸肠肠杆菌对肾脏血糖诱导大鼠肾脏氧化应激和炎症指标的影响评价

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INTRODUCTION: Sepsis is an important cause of mortality and morbidity, and inflammatory response and oxidative stress play major roles underlying its pathophysiology. Here, we evaluated the effect of intraperitoneal etanercept administration on oxidative stress and inflammation indicators in the kidney and blood of experimental sepsis-induced rats. METHODS: Twenty-eight adult Sprague Dawley rats were classified into Control (Group 1), Sepsis (Group 2), Sepsis+Cefazolin (Group 3), and Sepsis+Cefazolin+Etanercept (Group 4) groups. Kidney tissue and serum samples were obtained for biochemical and histopathological investigations and examined for the C reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), triggering receptor expressed on myeloid cells (TREM), and malondialdehyde (MDA) levels. RESULTS: The levels of TNF-α, TREM, and MDA in serum and kidney samples were significantly higher in rats from sepsis group than in rats from control group (p 0.05). Group 3 showed a significant reduction in serum levels of TNF-α, CRP, and TREM as compared with Group 2 (p 0.05). Serum TNF-α, CRP, TREM, and MDA levels and kidney TNF-α and TREM levels were significantly lower in Group 4 than in Group 2 (p 0.05). Serum TNF-α and TREM levels in Group 4 were significantly lower than those in Group 3, and histopathological scores were significantly lower in Group 3 and Group 4 than in Group 2 (p 0.05). Histopathological scores of Group 4 were significantly lower than those of Group 3 (p 0.05).CONCLUSIONS: Etanercept, a TNF-α inhibitor, may ameliorate sepsis-induced oxidative stress, inflammation, and histopathological damage.
机译:介绍:败血症是死亡率和发病率的重要原因,炎症反应和氧化应激在其病理生理学中起主要的作用。在此,我们评估了腹膜内乙酸伊烷基对肾脏和血糖诱导大鼠肾脏氧化应激和炎症指标的影响。方法:二十八名成人Sprague Dawley大鼠被分类为对照(第1组),Sepsis(第2组),Sepsis + Cefazolin(第3组)和Sepsis + Cefazolin + entanercept(第4组)组。获得生化和组织病理学研究的肾组织和血清样品,并检查C反应蛋白(CRP),肿瘤坏死因子-α(TNF-α),触发骨髓细胞(TREM)和丙二醛(MDA)水平的触发受体。结果:来自败血症组大鼠的TNF-α,TREM和MDA的水平显着高于来自对照组的大鼠大鼠(P <0.05)。第3组与第2组相比显示血清TNF-α,CRP和TREM的显着降低(P <0.05)。血清TNF-α,CRP,TREM和MDA水平和肾脏TNF-α和肾脏TNF-α和肾脏TNF-α和THR水平明显低于2组(P <0.05)。第4组中的血清TNF-α和TREM水平显着低于第3组,组织病理学分数在第3组和第4组中显着降低(P <0.05)。第4组组的组织病理学评分显着低于第3组(P <0.05)。结论:依那西普,一种TNF-α抑制剂,可能改善脓毒症诱导的氧化应激,炎症和组织病理学损伤。
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