阿达木单抗能否防止脂多糖诱发大鼠肾损伤的急性效应?

Acta cirurgica brasileira Pub Date : 2024-09-02 eCollection Date: 2024-01-01 DOI:10.1590/acb394624
Nuket Özkavruk Eliyatkın, Akif İşlek, Selim Durmaz, Fevzi Ayyıldız, Ömer Rahman
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引用次数: 0

摘要

目的:众所周知,脂多糖在急性肾损伤过程中起着重要作用。它能广泛激活炎症级联反应。肿瘤坏死因子(TNF)-α和白细胞介素(Il)-6是重要的促炎细胞因子,可在宿主反应中诱导其他细胞因子的产生。阿达木单抗可抑制 TNF-α、IL-1β 和 IL-6。我们的目的是评估阿达木单抗是否能防止脂多糖对大鼠肾组织的毒性:方法:成年雌性 Wistar 大鼠分为四组。对照组只进行腹腔注射生理盐水。阿达木单抗组注射阿达木单抗,连续两天。对于脂多糖组,给动物注射脂多糖(一剂量)。脂多糖-阿达木单抗组:动物在注射脂多糖前接受阿达木单抗治疗。测定组织病理学变化以及TNF-α和IL-6的免疫组化分析:结果:对照组和阿达木单抗组的病理变化和TNF-α或IL-6的免疫组化染色结果相似(P > 0.05)。与对照组相比,脂多糖组的肾组织扭曲特征明显增加(p < 0.001),TNF-α或IL-6的免疫组化染色也明显突出(0.003)。脂多糖-阿达木单抗组未发现严重病理特征,但在所有病例中均发现中度坏死(p = 0.003)。与脂多糖-阿达木单抗组相比,脂多糖组的TNF-α染色和IL-6染色明显突出(p = 0.013):结论:阿达木单抗具有抗炎特性,其预处理可能对实验性肾损伤具有保护作用。阿达木单抗可被视为脂多糖诱导的急性肾损伤的保护剂。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Can adalimumab prevent from acute effects of lipopolysaccharide induced renal injury in rats?

Purpose: Lipopolysaccharides is well-known in the acute renal injury process. It causes widespread activation of inflammatory cascades. Tumor necrosis factor (TNF)-α and interleukin (Il)-6 are essential proinflammatory cytokines that can induce the production of other cytokines in host response. Adalimumab suppresses TNF-α, IL-1β, and IL-6. We aimed to evaluate whether adalimumab would prevent the toxicity of lipopolysaccharide on the rat renal tissue.

Methods: Adult female Wistar rats were divided into four groups. To the control group, only intraperitoneal saline injection procedure was carried out. For adalimumab group, adalimumab was injected at a dose for two days. For lipopolysaccharide group, animals were injected with lipopolysaccharide (a dose). For lipopolysaccharide-adalimumab group, animals were given adalimumab treatment before the injection of lipopolysaccharide. Histopathological changes and immunohistochemical analysis for TNF-α and IL-6 were determined.

Results: The pathological changes and immunohistochemical staining for TNF-α or IL-6 were similar for control and adalimumab groups (p > 0.05). The lipopolysaccharide group had significantly higher distorted features in the renal tissues (p < 0.001), and also significantly prominent immunohistochemical staining for TNF-α or IL-6 (0.003), compared to the control group. No severe pathological feature was detected in the lipopolysaccharide-adalimumab group, but moderate necrosis was found in all cases (p = 0.003). TNF-α staining and IL-6 staining in the lipopolysaccharide group was found to significantly prominent compared to lipopolysaccharide-adalimumab group (p = 0.013).

Conclusions: Because of its anti-inflammatory property, adalimumab pretreatment may have protective effects on experimental kidney injury. Adalimumab could be considered as a protective agent to acute effects of lipopolysaccharide induced renal injury.

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