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本文引用的文献

1
Epidermal growth factor inhibits carbachol-stimulated canine parietal cell function via protein kinase C.表皮生长因子通过蛋白激酶C抑制卡巴胆碱刺激的犬壁细胞功能。
Gastroenterology. 1996 Feb;110(2):469-77. doi: 10.1053/gast.1996.v110.pm8566594.
2
Interleukin-1 and experimental gastric ulcer healing in the rat.白细胞介素-1与大鼠实验性胃溃疡愈合
J Physiol Pharmacol. 1993 Mar;44(1):23-9.
3
Epidermal growth factor and transforming growth factor-alpha directly inhibit parietal cell function through a similar mechanism.表皮生长因子和转化生长因子-α 通过相似机制直接抑制壁细胞功能。
J Pharmacol Exp Ther. 1993 Apr;265(1):308-13.
4
Stimulation of human T-cell proliferation by specific activation of the 75-kDa tumor necrosis factor receptor.通过75 kDa肿瘤坏死因子受体的特异性激活刺激人T细胞增殖。
J Immunol. 1993 Nov 1;151(9):4637-41.
5
Distribution of Helicobacter pylori colonisation and associated gastric inflammatory changes: difference between patients with duodenal and gastric ulcers.幽门螺杆菌定植分布及相关胃炎症变化：十二指肠溃疡与胃溃疡患者之间的差异
J Clin Pathol. 1993 Aug;46(8):754-6. doi: 10.1136/jcp.46.8.754.
6
Mucosal tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-8 production in patients with Helicobacter pylori infection.幽门螺杆菌感染患者黏膜肿瘤坏死因子-α、白细胞介素-1β和白细胞介素-8的产生
Scand J Gastroenterol. 1994 May;29(5):425-9. doi: 10.3109/00365529409096833.
7
Helicobacter pylori.幽门螺杆菌
Eur J Clin Invest. 1994 Aug;24(8):501-10. doi: 10.1111/j.1365-2362.1994.tb01099.x.
8
Multiple actions of epidermal growth factor and TGF-alpha on rabbit gastric parietal cell function.表皮生长因子和转化生长因子-α对兔胃壁细胞功能的多种作用。
Am J Physiol. 1994 Nov;267(5 Pt 1):G818-26. doi: 10.1152/ajpgi.1994.267.5.G818.
9
Interleukin-1 beta inhibits gastric histamine secretion and synthesis in the rat.白细胞介素-1β抑制大鼠胃组胺的分泌和合成。
Am J Physiol. 1994 Dec;267(6 Pt 1):G966-71. doi: 10.1152/ajpgi.1994.267.6.G966.
10
Helicobacter pylori infection and abnormalities of acid secretion in patients with duodenal ulcer disease.十二指肠溃疡病患者的幽门螺杆菌感染与胃酸分泌异常
Gastroenterology. 1995 Sep;109(3):681-91. doi: 10.1016/0016-5085(95)90374-7.

白细胞介素1β和肿瘤坏死因子α通过多种途径抑制培养的兔壁细胞的酸分泌。

Interleukin 1 beta and tumour necrosis factor alpha inhibit acid secretion in cultured rabbit parietal cells by multiple pathways.

作者信息

Beales I L, Calam J

机构信息

Department of Gastroenterology, Royal Postgraduate Medical School, Hammersmith Hospital, London, UK.

出版信息

Gut. 1998 Feb;42(2):227-34. doi: 10.1136/gut.42.2.227.

DOI:10.1136/gut.42.2.227
PMID:9536948
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1726991/
Abstract

BACKGROUND

The cytokines interleukin 1 beta (IL-1 beta) and tumour necrosis factor alpha (TNF-alpha) are inhibitors of gastric acid secretion when administered systemically.

AIMS

To investigate the inhibitory effect of IL-1 beta and TNF-alpha on cultured, acid secreting parietal cells in order to determine the mechanism of this inhibition.

METHODS

Rabbit parietal cells were prepared by collagenase-EDTA digestion and counter flow elutriation. Acid secretory activity was assessed by aminopyrine accumulation.

RESULTS

IL-1 beta and TNF-alpha inhibited basal and stimulated acid secretion in a dose dependent manner; near maximal effects were seen with both at 10 ng/ml. Inhibition was maximal with 15 minutes pretreatment but seen with up to 18 hours of preincubation. Both cytokines inhibited histamine, carbachol, gastrin, forskolin, and A23187 stimulated acid secretion but had no effect on stimulation by dibutyryl-cAMP. Inhibition of acid secretion was not accompanied by a change in radioligand binding to histamine H2 or gastrin/CCKB receptors. Pertussis toxin abolished the inhibitory effects on histamine and forskolin stimulation. The tyrosine kinase inhibitor herbimycin reduced the inhibitory effects of TNF-alpha against all stimuli but only reduced the effects of IL-1 beta against histamine and forskolin stimulation.

CONCLUSIONS

IL-1 beta and TNF-alpha seem to inhibit parietal cell acid secretion by multiple pathways; the inhibition occurs at postreceptor level and involves pertussis toxin and tyrosine kinase dependent and independent pathways. Mucosal production of cytokines may be important in the regulation of gastric acid secretion.

摘要

背景

细胞因子白细胞介素1β（IL-1β）和肿瘤坏死因子α（TNF-α）全身给药时是胃酸分泌的抑制剂。

目的

研究IL-1β和TNF-α对培养的泌酸壁细胞的抑制作用，以确定这种抑制的机制。

方法

通过胶原酶-乙二胺四乙酸消化和逆流淘析制备兔壁细胞。通过氨基比林蓄积评估酸分泌活性。

结果

IL-1β和TNF-α以剂量依赖方式抑制基础和刺激的酸分泌；二者在10 ng/ml时均可见接近最大效应。预处理15分钟时抑制作用最大，但预孵育长达18小时也可见抑制作用。两种细胞因子均抑制组胺、卡巴胆碱、胃泌素、福斯可林和A23187刺激的酸分泌，但对二丁酰环磷腺苷刺激无影响。酸分泌的抑制并未伴随放射性配体与组胺H2或胃泌素/CCKB受体结合的改变。百日咳毒素消除了对组胺和福斯可林刺激的抑制作用。酪氨酸激酶抑制剂赫曲霉素降低了TNF-α对所有刺激的抑制作用，但仅降低了IL-1β对组胺和福斯可林刺激的抑制作用。

结论

IL-1β和TNF-α似乎通过多种途径抑制壁细胞酸分泌；抑制发生在受体后水平，涉及百日咳毒素以及酪氨酸激酶依赖性和非依赖性途径。细胞因子的黏膜产生在胃酸分泌调节中可能很重要。