{"title":"胞内钙在脂多糖刺激Kupffer细胞产生超氧阴离子中的作用及前列腺素E1的作用","authors":"Haruki Kurosawa , Hiroshi Shimada, Akira Nakano, Shiho Natori, Yuichi Fujii","doi":"10.1016/0928-4346(96)00264-2","DOIUrl":null,"url":null,"abstract":"<div><p>Kupffer cells stimulated by lipopolysaccharide (LPS) produce Superoxide anion and cause hepatocellular injury. Intracellular calcium has been noted to work as a second messenger in a variety of pathophysiological mechanisms. The aims of this study were to investigate the effect of LPS stimulation of Kupffer cells on intracellular calcium concentrations and the production of Superoxide anion, and determine the effect of prostaglandin E<sub>1</sub> (PGE<sub>1</sub>) on intracellular calcium and the Superoxide anion production following stimulation with LPS. Kupffer cells were isolated from male Wistar rats. The intracellular calcium level and the production of Superoxide anion were measured using a fluorescence computed microscope (Mu-1000, Inter Dec) and a Luminescence Reader (BLR-103, Aloka). After LPS stimulation, the intracellular calcium level of Kupffer cells increased and pretreatment with PGE<sub>1</sub> reduced this increase. Pretreatment with PGE<sub>1</sub> and removal of extracellular calcium decreased the production of Superoxide anion from Kupffer cells stimulated by LPS. We conclude that an increase of intracellular calcium affects production of Superoxide anion from Kupffer cells stimulated by LPS. Pretreatment with PGE<sub>1</sub> reduces the production of Superoxide anion by preventing this rise in intracellular calcium.</p></div>","PeriodicalId":13746,"journal":{"name":"International Hepatology Communications","volume":"4 6","pages":"Pages 326-333"},"PeriodicalIF":0.0000,"publicationDate":"1996-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0928-4346(96)00264-2","citationCount":"6","resultStr":"{\"title\":\"The role of intracellular calcium in the production of Superoxide anion by Kupffer cells stimulated by lipopolysaccharide and the efficacy of prostaglandin E1\",\"authors\":\"Haruki Kurosawa , Hiroshi Shimada, Akira Nakano, Shiho Natori, Yuichi Fujii\",\"doi\":\"10.1016/0928-4346(96)00264-2\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>Kupffer cells stimulated by lipopolysaccharide (LPS) produce Superoxide anion and cause hepatocellular injury. Intracellular calcium has been noted to work as a second messenger in a variety of pathophysiological mechanisms. The aims of this study were to investigate the effect of LPS stimulation of Kupffer cells on intracellular calcium concentrations and the production of Superoxide anion, and determine the effect of prostaglandin E<sub>1</sub> (PGE<sub>1</sub>) on intracellular calcium and the Superoxide anion production following stimulation with LPS. Kupffer cells were isolated from male Wistar rats. The intracellular calcium level and the production of Superoxide anion were measured using a fluorescence computed microscope (Mu-1000, Inter Dec) and a Luminescence Reader (BLR-103, Aloka). After LPS stimulation, the intracellular calcium level of Kupffer cells increased and pretreatment with PGE<sub>1</sub> reduced this increase. Pretreatment with PGE<sub>1</sub> and removal of extracellular calcium decreased the production of Superoxide anion from Kupffer cells stimulated by LPS. We conclude that an increase of intracellular calcium affects production of Superoxide anion from Kupffer cells stimulated by LPS. Pretreatment with PGE<sub>1</sub> reduces the production of Superoxide anion by preventing this rise in intracellular calcium.</p></div>\",\"PeriodicalId\":13746,\"journal\":{\"name\":\"International Hepatology Communications\",\"volume\":\"4 6\",\"pages\":\"Pages 326-333\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1996-04-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/0928-4346(96)00264-2\",\"citationCount\":\"6\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"International Hepatology Communications\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/0928434696002642\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"International Hepatology Communications","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/0928434696002642","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 6
摘要
脂多糖刺激库普弗细胞产生超氧阴离子，引起肝细胞损伤。细胞内钙在多种病理生理机制中被认为是第二信使。本研究旨在探讨LPS刺激Kupffer细胞对细胞内钙浓度和超氧阴离子产生的影响，并确定LPS刺激后前列腺素E1 (PGE1)对细胞内钙和超氧阴离子产生的影响。从雄性Wistar大鼠中分离Kupffer细胞。使用荧光计算机显微镜(Mu-1000, Inter Dec)和发光阅读器(BLR-103, Aloka)测量细胞内钙水平和超氧阴离子的产生。LPS刺激后，Kupffer细胞内钙水平升高，PGE1预处理降低了这种升高。PGE1预处理和去除细胞外钙降低了LPS刺激下Kupffer细胞超氧阴离子的产生。我们得出的结论是，细胞内钙的增加影响了LPS刺激下Kupffer细胞超氧阴离子的产生。PGE1预处理通过防止细胞内钙的增加减少了超氧阴离子的产生。
The role of intracellular calcium in the production of Superoxide anion by Kupffer cells stimulated by lipopolysaccharide and the efficacy of prostaglandin E1
Kupffer cells stimulated by lipopolysaccharide (LPS) produce Superoxide anion and cause hepatocellular injury. Intracellular calcium has been noted to work as a second messenger in a variety of pathophysiological mechanisms. The aims of this study were to investigate the effect of LPS stimulation of Kupffer cells on intracellular calcium concentrations and the production of Superoxide anion, and determine the effect of prostaglandin E1 (PGE1) on intracellular calcium and the Superoxide anion production following stimulation with LPS. Kupffer cells were isolated from male Wistar rats. The intracellular calcium level and the production of Superoxide anion were measured using a fluorescence computed microscope (Mu-1000, Inter Dec) and a Luminescence Reader (BLR-103, Aloka). After LPS stimulation, the intracellular calcium level of Kupffer cells increased and pretreatment with PGE1 reduced this increase. Pretreatment with PGE1 and removal of extracellular calcium decreased the production of Superoxide anion from Kupffer cells stimulated by LPS. We conclude that an increase of intracellular calcium affects production of Superoxide anion from Kupffer cells stimulated by LPS. Pretreatment with PGE1 reduces the production of Superoxide anion by preventing this rise in intracellular calcium.
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