{"title":"OK-432抑制MRL/lpr小鼠自身免疫性肾病的研究2吲哚美辛的效果。","authors":"M Mihara, Y Ohsugi","doi":"10.1248/bpb1978.15.255","DOIUrl":null,"url":null,"abstract":"<p><p>We have reported that OK-432 (a streptococcal preparation) prevents the development of autoimmune kidney disease in MRL/Mp-lpr/lpr (MRL/lpr) mice and prolongs their survival time. In the present study, to clarify the mechanism of this action of OK-432, we examined whether the cyclooxygenase inhibitor indomethacin (IND) affects this inhibition by OK-432. It was reconfirmed that OK-432 prevented the development of autoimmune kidney disease and prolonged the survival time. This OK-432 effect was counteracted when IND was coadministered. Furthermore, OK-432 produced tumor necrosis factor (TNF)-alpha and prostaglandin (PG) E2 in the peritoneal fluids in this strain of mice. The coadministration of IND suppressed the PGE2 but not the TNF-alpha production. These results suggest the possibility that the inhibition of autoimmune kidney disease by OK-432 might be due to the induction of cyclooxygenase metabolites of arachidonic acid.</p>","PeriodicalId":16743,"journal":{"name":"Journal of pharmacobio-dynamics","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1992-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1248/bpb1978.15.255","citationCount":"1","resultStr":"{\"title\":\"Autoimmune kidney disease in MRL/lpr mice inhibited by OK-432; II. Effect of indomethacin.\",\"authors\":\"M Mihara, Y Ohsugi\",\"doi\":\"10.1248/bpb1978.15.255\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>We have reported that OK-432 (a streptococcal preparation) prevents the development of autoimmune kidney disease in MRL/Mp-lpr/lpr (MRL/lpr) mice and prolongs their survival time. In the present study, to clarify the mechanism of this action of OK-432, we examined whether the cyclooxygenase inhibitor indomethacin (IND) affects this inhibition by OK-432. It was reconfirmed that OK-432 prevented the development of autoimmune kidney disease and prolonged the survival time. This OK-432 effect was counteracted when IND was coadministered. Furthermore, OK-432 produced tumor necrosis factor (TNF)-alpha and prostaglandin (PG) E2 in the peritoneal fluids in this strain of mice. The coadministration of IND suppressed the PGE2 but not the TNF-alpha production. These results suggest the possibility that the inhibition of autoimmune kidney disease by OK-432 might be due to the induction of cyclooxygenase metabolites of arachidonic acid.</p>\",\"PeriodicalId\":16743,\"journal\":{\"name\":\"Journal of pharmacobio-dynamics\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1992-05-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1248/bpb1978.15.255\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of pharmacobio-dynamics\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1248/bpb1978.15.255\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of pharmacobio-dynamics","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1248/bpb1978.15.255","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Autoimmune kidney disease in MRL/lpr mice inhibited by OK-432; II. Effect of indomethacin.
We have reported that OK-432 (a streptococcal preparation) prevents the development of autoimmune kidney disease in MRL/Mp-lpr/lpr (MRL/lpr) mice and prolongs their survival time. In the present study, to clarify the mechanism of this action of OK-432, we examined whether the cyclooxygenase inhibitor indomethacin (IND) affects this inhibition by OK-432. It was reconfirmed that OK-432 prevented the development of autoimmune kidney disease and prolonged the survival time. This OK-432 effect was counteracted when IND was coadministered. Furthermore, OK-432 produced tumor necrosis factor (TNF)-alpha and prostaglandin (PG) E2 in the peritoneal fluids in this strain of mice. The coadministration of IND suppressed the PGE2 but not the TNF-alpha production. These results suggest the possibility that the inhibition of autoimmune kidney disease by OK-432 might be due to the induction of cyclooxygenase metabolites of arachidonic acid.
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