Prevention by lansoprazole, a proton pump inhibitor, of indomethacin -induced small intestinal ulceration in rats through induction of heme oxygenase-1.
Prevention by lansoprazole, a proton pump inhibitor, of indomethacin -induced small intestinal ulceration in rats through induction of heme oxygenase-1.
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兰索拉唑（一种质子泵抑制剂）通过诱导血红素加氧酶-1 来预防吲哚美辛诱导的大鼠小肠溃疡。
DOI：
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发表时间：
2010
影响因子：
2.2
通讯作者：
K. Higuchi
中科院分区：
文献类型：
--
作者：
Y. Yoda;K. Amagase;S. Kato;S. Tokioka;M. Murano;K. Kakimoto;H. Nishio;E. Umegaki;K. Takeuchi;K. Higuchi
观察了质子泵抑制剂(PPI)兰索拉唑对消炎痛诱导的大鼠小肠溃疡的影响，特别是与血红素加氧酶(HO)-1的关系。给动物注射消炎痛(10 mg/kg，P.O.)。24小时后被杀。兰索拉唑(30-100 mg/kg，P.O.)和奥美拉唑(30-100 mg/kg，P.O.)在给予消炎痛或兰索拉唑前10分钟静脉注射HO-1抑制剂锡原卟啉IX(SnPP：30 mg/kg)。吲哚美辛造成小肠出血性病变，并伴有肠杆菌的黏膜侵袭增加，粘膜诱导型一氧化氮合酶(INOS)表达和髓过氧化酶(MPO)活性增加。兰索拉唑可剂量依赖性地减轻吲哚美辛诱导的肠道损伤，抑制MPO活性的升高，而奥美拉唑对此无影响。预先给予SnPP可明显加重上述肠道损伤，并几乎完全消除兰索拉唑的保护作用。兰索拉唑可抑制吲哚美辛诱导的iNOS mRNA表达上调，但抑制SnPP对肠道细菌侵袭的增强作用。兰索拉唑能显著增加肠粘膜HO-1蛋白的含量，而奥美拉唑对此无明显影响。预先给予一氧化碳(CO)释放分子-2(CORM-2；10 mg/kg，i.p.)显著减轻吲哚美辛诱导的小肠粘膜iNOS mRNA表达增强及上述病变的严重程度。上述结果提示，兰索拉唑可通过上调HO-1/CO的生成，抑制iNOS的表达，从而预防消炎痛所致的小肠溃疡。
The effect of lansoprazole, a proton pump inhibitor (PPI), on indomethacin-induced small intestinal ulceration was examined in rats, particularly in relation to heme oxygenase (HO)-1. The animals were administered indomethacin (10 mg/kg, p.o.) and killed 24 h later. Lansoprazole (30-100 mg/kg, p.o.) and omeprazole (30-100 mg/kg, p.o.) were given 30 min before the administration of indomethacin, while tin-protoporphyrin IX (SnPP: 30 mg/kg, i.v.), an inhibitor of HO-1, was injected 10 min before indomethacin or lansoprazole. Indomethacin produced hemorrhagic lesions in the small intestine, accompanied with an increase of mucosal invasion of enterobacteria, inducible nitric oxide synthase (iNOS) expression, and myeloperoxidase (MPO) activity in the mucosa. Pretreatment with lansoprazole dose- dependently reduced the severity of the indomethacin-induced intestinal lesions, with suppression of the increased MPO activity, while omeprazole had no effect. Pretreatment with SnPP significantly exacerbated these intestinal lesions and almost totally abolished the protective effect of lansoprazole. The up-regulation of iNOS mRNA expression following indomethacin was suppressed by lansoprazole in a SnPP-inhibitable manner, although the enhanced enterobacterial invasion remained unaffected. The amount of HO-1 protein in the intestinal mucosa was significantly increased by lansoprazole but not by omeprazole. Prior administration of carbon monoxide (CO)-releasing molecule-2 (CORM-2; 10 mg/kg, i.p.) significantly reduced the severity of these lesions and the enhancement of mucosal iNOS mRNA expression induced in the small intestine by indomethacin. These results suggest that lansoprazole prevents indomethacin-induced small intestinal ulceration, and this effect is associated with inhibition of iNOS expression, through up-regulation of HO-1/CO production in the mucosa.
释放一氧化碳的化合物对缺血引起的急性肾衰竭的保护作用。
DOI：
10.1681/asn.2004090736
发表时间：
2005
期刊：
Journal of the American Society of Nephrology : JASN
影响因子：
--
作者：
Vera,Trinity;Henegar,JefferyR;Drummond,HeatherA;Rimoldi,JohnM;Stec,DavidE
通讯作者：
Stec,DavidE
影响因子：
29.4
作者：
J. E. Krawisz;P. Sharon;W. Stenson
通讯作者：
J. E. Krawisz;P. Sharon;W. Stenson