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硼酸和 2-氨乙氧基二苯硼酸盐对坏死性小肠结肠炎的影响。

Effects of boric acid and 2-aminoethoxydiphenyl borate on necrotizing enterocolitis.

机构信息

*Department of Pediatrics, Medical Faculty †Department of Biochemistry, Faculty of Veterinary Medicine ‡Department of Pharmachology §Department of Histology, Balıkesir University, Medical Faculty, Balıkesir ||Department of Pediatrics, Ministry of Health, Dr Behçet Uz Pediatric Hospital, İzmir, Turkey.

出版信息

J Pediatr Gastroenterol Nutr. 2014 Jan;58(1):61-7. doi: 10.1097/MPG.0b013e3182a7e02b.

Abstract

OBJECTIVE

The aim was to study the effects of boric acid (BA) and 2-aminoethoxydiphenyl borate (2-APB) on oxidative stress and inflammation in an experimental necrotizing enterocolitis (NEC) rat model.

METHODS

Experimental NEC was induced in 40 newborn Sprague-Dawley rats by asphyxia and hypothermia applied in 3 consecutive days. Rats were subdivided into 4 subgroups as NEC, NEC+BA, NEC+2-APB, and controls. BA and 2-APB were applied daily before the procedure. Serum total antioxidant status, superoxide dismutase (SOD), tumor necrosis factor (TNF)-α, interleukin (IL)-6, and erythrocyte glutathione (GSH) levels were measured. Pathological changes for NEC in intestinal architecture were evaluated by a grading system.

RESULTS

Pretreatment with BA and 2-APB resulted in a decrease in NEC incidence. In all of the NEC groups, decreased serum levels of GSH and SOD were measured. Boron limited GSH consumption but had no effect on SOD levels. Total antioxidant status levels were not statistically different among groups. In our experimental NEC model, BA, but not 2-APB, prevented the increase of TNF-α. Pretreatment with BA and 2-APB downregulated the activity levels of IL-6 in NEC.

CONCLUSIONS

In the experimental NEC model, BA and 2-APB partly prevent NEC formation, modulate the oxidative stress parameters, bring a significant decrease in GSH consumption, and enhance the antioxidant defense mechanism, but have no effect on total antioxidant status. BA inhibits the hypoxia and hypothermia-induced increase in both IL-6 and TNF-a, but 2-APB only in IL-6. Boron may be beneficial in preventing NEC.

摘要

目的

研究硼酸(BA)和 2-氨乙氧基二苯硼酸盐(2-APB)对实验性坏死性小肠结肠炎(NEC)大鼠模型氧化应激和炎症的影响。

方法

通过连续 3 天的窒息和低温处理,使 40 只新生 Sprague-Dawley 大鼠产生实验性 NEC。大鼠分为 NEC、NEC+BA、NEC+2-APB 和对照组 4 组。在手术前每天给予 BA 和 2-APB。测定血清总抗氧化状态、超氧化物歧化酶(SOD)、肿瘤坏死因子(TNF)-α、白细胞介素(IL)-6 和红细胞谷胱甘肽(GSH)水平。通过分级系统评估肠道结构的 NEC 病理变化。

结果

BA 和 2-APB 预处理可降低 NEC 发生率。在所有 NEC 组中,均发现 GSH 和 SOD 血清水平降低。硼限制 GSH 消耗,但对 SOD 水平无影响。各组之间总抗氧化状态水平无统计学差异。在我们的实验性 NEC 模型中,BA 而不是 2-APB 可防止 TNF-α的增加。BA 和 2-APB 预处理可降低 NEC 中 IL-6 的活性水平。

结论

在实验性 NEC 模型中,BA 和 2-APB 部分预防 NEC 的形成,调节氧化应激参数,显著减少 GSH 的消耗,并增强抗氧化防御机制,但对总抗氧化状态无影响。BA 抑制缺氧和低温诱导的 IL-6 和 TNF-α的增加,但 2-APB 仅抑制 IL-6。硼可能有益于预防 NEC。

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