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β-胡萝卜素在盐酸模型中诱导胃细胞保护作用的自由基机制。

The free radical mechanisms in beta-carotene induced gastric cytoprotection in HCl model.

作者信息

Vincze A, Garamszegi M, Jávor T, Sütö G, Tigyi A, Tóth G, Zsoldos T, Mózsik G

机构信息

First Department of Medicine, University Medical School, Pécs, Hungary.

出版信息

Acta Physiol Hung. 1989;73(2-3):351-5.

PMID:2596322
Abstract

The aims of our experiments were to clear up the possible correlations between the free radical mechanisms and the gastric cytoprotection of beta-carotene on HCl-induced gastric mucosal lesions. The beta-carotene was intragastrically given in doses of 1 and 10 mg/kg and 30 min. later 1 ml 0.6 N HCl was given to provoke the mucosal damage. After 1, 5, 15, 30 and 60 min. the animals were sacrificed. The number and severity of gastric mucosal lesions were calculated. The superoxide dismutase (SOD), glutathion peroxidase (GPX), catalase (CAT) activity and the malondialdehyde (MDA) and reduced glutathion (GSH) contents were determined from the gastric mucosa of rats. It was found that 1. beta-carotene was able to reduce the number and severity of ulcers only after 30 min.; 2. the CAT activity was decreased at 60 min. by carotene; 3. the GPX activity became dissimilar in the different groups after 15 min; 4. the changes of GSH were found to be similar ones; 5. the SOD activity was lower during the cyto-protection; 6. the MDA level remained practically unchanged. It has been concluded that 1. the free radicals are the consequences of the development of gastric ulcer and cytoprotection; 2. the scavenger character of beta-carotene is involved in its cytoprotective effect.

摘要

我们实验的目的是明确自由基机制与β-胡萝卜素对盐酸诱导的胃黏膜损伤的胃细胞保护作用之间可能存在的相关性。以1和10mg/kg的剂量胃内给予β-胡萝卜素,30分钟后给予1ml 0.6N盐酸以引发黏膜损伤。1、5、15、30和60分钟后处死动物。计算胃黏膜损伤的数量和严重程度。测定大鼠胃黏膜中的超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GPX)、过氧化氢酶(CAT)活性以及丙二醛(MDA)和还原型谷胱甘肽(GSH)含量。结果发现:1. β-胡萝卜素仅在30分钟后能够减少溃疡的数量和严重程度;2. 60分钟时胡萝卜素使CAT活性降低;3. 15分钟后不同组间GPX活性出现差异;4. 发现GSH的变化情况类似;5. 细胞保护期间SOD活性较低;6. MDA水平基本保持不变。得出的结论是:1. 自由基是胃溃疡发生和细胞保护的结果;2. β-胡萝卜素的清除自由基特性参与了其细胞保护作用。

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