Could honey have a place in colitis therapy? Effects of honey, prednisolone, and disulfiram on inflammation, nitric oxide, and free radical formation
Could honey have a place in colitis therapy? Effects of honey, prednisolone, and disulfiram on inflammation, nitric oxide, and free radical formation
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DOI：
10.1159/000064580
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发表时间：
2002-01-01
影响因子：
2.7
通讯作者：
Turkoglu, U
中科院分区：
文献类型：
--
作者：
Bilsel, Y;Bugra, D;Turkoglu, U
背景/目标：本研究的目的是探讨蜂蜜，泼尼松龙和双硫仑在炎症性肠病实验模型中的潜在治疗作用。这项研究的另一个方面是找出这些物质是否对一氧化氮（NO）和自由基的产生有任何影响。研究方法：在64只雄性大鼠中用三硝基苯磺酸诱导结肠炎后，每天一次对大鼠应用生理盐水、蜂蜜、泼尼松龙和双硫仑灌肠，连续3d（急性治疗组）或7d（慢性治疗组）。对照组仅给予生理盐水灌肠。在第4天或第8天处死大鼠，使用评分系统定量其结肠粘膜损伤。急性和慢性炎症反应通过粘膜损伤评分、组织学检查和组织髓过氧化物酶（MPO）活性测定来确定。测定结肠组织匀浆中丙二醛（MIDA）和NO代谢产物的含量，以评估这些物质对NO和自由基产生的影响。结果：通过粘膜损伤评分评估结肠损伤与结肠标本的组织学评价密切相关。另一方面，粘膜损伤评分与MPO、MDA或NO值无关。慢性对照组和慢性蜂蜜组以及慢性对照组和慢性泼尼松龙组的MPO结果之间存在显著差异（p = 0.03和p = 0.0007）。与急性对照组相比，急性蜂蜜、泼尼松龙和双硫仑组的MDA结果显著较低（p = 0.04、p = 0.02和p = 0.04）。在NO方面，治疗组与对照组之间无显著差异。发现NO与MDA（p = 0.03）和MPO值（p = 0.001）具有强相关性。另一方面，未发现MPO结果与MDA值相关（p> 0.05）。结论：MPO活性与炎症的严重程度不成正比，但它可能仅决定组织中中性粒细胞的数量。炎症细胞不是结肠炎的唯一强化因素。因此，粘膜损伤评分可能与MPO活性不相关。在炎症状态下，NO和MPO水平具有很强的相关性，因为NO是从中性粒细胞释放的。在结肠炎的炎症模型中，直肠内蜂蜜给药与泼尼松龙治疗一样有效。蜂蜜在治疗结肠炎方面可能有一些特点，但这个问题需要进一步研究。蜂蜜，泼尼松龙，甚至双硫仑也有一定的价值，在防止自由基的形成释放的发炎组织。泼尼松龙也可能在结肠炎治疗中抑制NO产生方面具有一些可能的益处。版权所有（C）2002 S. Karger AG，巴塞尔。
Background/Aims: The purpose of this study was to investigate the potential therapeutic roles of honey, prednisolone and disulfiram in an experimental model of inflammatory bowel disease. Another aspect of the study was to find out whether these substances have any effect on nitric oxide (NO) and free radical production. Methods: After the induction of colitis with trinitrobenzene sulfonic acid in 64 male rats, physiological saline, honey, prednisolone and disulfiram enemas were applied to the rats once daily for 3 days (acute treatment groups) or 7 days (chronic treatment groups). Control groups received only saline enemas. Rats were killed on the 4th or 8th days and their colonic mucosal damage was quantitated using a scoring system. Acute and chronic inflammatory responses were determined by a mucosal injury score, histological examination and measurement of the myeloperoxidase (MPO) activity of tissues. The content of malonylaldehyde (MIDA) and NO metabolites in colon homogenates was also measured to assess the effects of these substances on NO and free oxygen radical production. Results: Estimation of colonic damage by mucosal injury scoring was found to be strongly correlated with the histologic evaluation of colon specimens. On the other hand, mucosal injury scores were not correlated with MPO, MDA or NO values. There were significant differences between the MPO results of chronic-control and chronic-honey groups, as well as chronic-control and chronic-prednisolone groups (p = 0.03 and p = 0.0007). The acute honey, prednisolone, and disulfiram groups had significantly lower MDA results compared to the acute control group (p = 0.04, p = 0.02, and p = 0.04). In terms of NO, there was no significant difference between the treatment and control groups. NO was found to have a strong relationship with MDA (p = 0.03) and MPO values (p = 0.001). On the other hand, MPO results were not found to be correlated with MDA values (p > 0.05). Conclusions: MPO activity is not directly proportional to the severity of the inflammation, but it may only determine the amount of neutrophil in the tissues. Inflammatory cells are not the sole intensifying factor in colitis. Therefore, mucosal injury scores may not correlate well with MPO activities. In an inflammatory state NO and MPO levels have a strong relationship, since NO is released from the neutrophils. In an inflammatory model of colitis, intrarectal honey administration is as effective as prednisolone treatment. Honey may have some features in the treatment of colitis, but this issue requires further investigation. Honey, prednisolone and even disulfiram also have some value in preventing the formation of free radicals released from the inflamed tissues. Prednisolone may also have some possible benefits in the inhibition of NO production in colitis therapy. Copyright (C) 2002 S. Karger AG, Basel.