Fitriana Fitriana, Soetrisno Soetrisno, Sri Sulistyowati, Dono Indarto
{"title":"评估 L-NAME 诱导的早发型子痫前期(EO-PE)大鼠模型的胎盘子宫床。","authors":"Fitriana Fitriana, Soetrisno Soetrisno, Sri Sulistyowati, Dono Indarto","doi":"10.4274/tjod.galenos.2024.99132","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>Preeclampsia (PE) is the leading cause of maternal death worldwide and is associated with long-term morbidity in both mothers and newborns. Animal modeling is considered a functional source for understanding PE pathogenesis, diagnostic standards, and therapeutic approaches.</p><p><strong>Materials and methods: </strong>This study aimed to demonstrate and evaluate the use of N-nitro-L-arginine methyl ester (L-NAME) in a Wistar rat model under conditions similar to PE. A total of 12 rats were divided into 4 groups, each consisting of 3 members, including the pregnant control group and treatment groups administered low-dose (PE 25 mg/kg L-NAME/day), medium-dose (PE 50 mg/kg L-NAME/day), and high-dose L-NAME (PE 75 mg/kg L-NAME/day) L-NAME from gestational day 4 to 19. Measurements included blood pressure, creatinine, and proteinuria levels, placental histological changes, and placental tissue hypoxia-inducible factor 1-alpha, and plasma endothelial nitric oxide synthase levels.</p><p><strong>Results: </strong>The results showed that intervention with L-NAME at 75 mg/kg body weight/day (PE3) induced PE earlier than that with 50 mg/kg body weight/day L-NAME.</p><p><strong>Conclusion: </strong>The model conditions also support further research into PE pathogenesis.</p>","PeriodicalId":45340,"journal":{"name":"Turkish Journal of Obstetrics and Gynecology","volume":"21 3","pages":"180-189"},"PeriodicalIF":1.0000,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11589322/pdf/","citationCount":"0","resultStr":"{\"title\":\"Evaluation of placental bed uterine in L-NAME-induced early-onset preeclampsia (EO-PE) like the rat model.\",\"authors\":\"Fitriana Fitriana, Soetrisno Soetrisno, Sri Sulistyowati, Dono Indarto\",\"doi\":\"10.4274/tjod.galenos.2024.99132\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>Preeclampsia (PE) is the leading cause of maternal death worldwide and is associated with long-term morbidity in both mothers and newborns. Animal modeling is considered a functional source for understanding PE pathogenesis, diagnostic standards, and therapeutic approaches.</p><p><strong>Materials and methods: </strong>This study aimed to demonstrate and evaluate the use of N-nitro-L-arginine methyl ester (L-NAME) in a Wistar rat model under conditions similar to PE. A total of 12 rats were divided into 4 groups, each consisting of 3 members, including the pregnant control group and treatment groups administered low-dose (PE 25 mg/kg L-NAME/day), medium-dose (PE 50 mg/kg L-NAME/day), and high-dose L-NAME (PE 75 mg/kg L-NAME/day) L-NAME from gestational day 4 to 19. Measurements included blood pressure, creatinine, and proteinuria levels, placental histological changes, and placental tissue hypoxia-inducible factor 1-alpha, and plasma endothelial nitric oxide synthase levels.</p><p><strong>Results: </strong>The results showed that intervention with L-NAME at 75 mg/kg body weight/day (PE3) induced PE earlier than that with 50 mg/kg body weight/day L-NAME.</p><p><strong>Conclusion: </strong>The model conditions also support further research into PE pathogenesis.</p>\",\"PeriodicalId\":45340,\"journal\":{\"name\":\"Turkish Journal of Obstetrics and Gynecology\",\"volume\":\"21 3\",\"pages\":\"180-189\"},\"PeriodicalIF\":1.0000,\"publicationDate\":\"2024-09-04\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11589322/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Turkish Journal of Obstetrics and Gynecology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.4274/tjod.galenos.2024.99132\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"OBSTETRICS & GYNECOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Turkish Journal of Obstetrics and Gynecology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4274/tjod.galenos.2024.99132","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"OBSTETRICS & GYNECOLOGY","Score":null,"Total":0}
Evaluation of placental bed uterine in L-NAME-induced early-onset preeclampsia (EO-PE) like the rat model.
Objective: Preeclampsia (PE) is the leading cause of maternal death worldwide and is associated with long-term morbidity in both mothers and newborns. Animal modeling is considered a functional source for understanding PE pathogenesis, diagnostic standards, and therapeutic approaches.
Materials and methods: This study aimed to demonstrate and evaluate the use of N-nitro-L-arginine methyl ester (L-NAME) in a Wistar rat model under conditions similar to PE. A total of 12 rats were divided into 4 groups, each consisting of 3 members, including the pregnant control group and treatment groups administered low-dose (PE 25 mg/kg L-NAME/day), medium-dose (PE 50 mg/kg L-NAME/day), and high-dose L-NAME (PE 75 mg/kg L-NAME/day) L-NAME from gestational day 4 to 19. Measurements included blood pressure, creatinine, and proteinuria levels, placental histological changes, and placental tissue hypoxia-inducible factor 1-alpha, and plasma endothelial nitric oxide synthase levels.
Results: The results showed that intervention with L-NAME at 75 mg/kg body weight/day (PE3) induced PE earlier than that with 50 mg/kg body weight/day L-NAME.
Conclusion: The model conditions also support further research into PE pathogenesis.