{"title":"在精氨酸加压素诱导的子痫前期大鼠模型中，肾功能障碍是否会加重？","authors":"Sapna Ramdin , Thajasvarie Naicker , Sooraj Baijnath , Nalini Govender","doi":"10.1016/j.repbio.2024.100910","DOIUrl":null,"url":null,"abstract":"<div><p>Renal dysfunction is important in preeclampsia (PE) pathophysiology and has not been fully explored in the arginine vasopressin (AVP) rat model of PE. This study aimed to determine kidney toxicity associated with this model. Female Sprague Dawley rats (n = 24) were subcutaneously infused with AVP or saline for 18 days. Urine samples (GD8, 14 and 18) were used to determine the levels of albumin, VEGF-A, clusterin, NGAL/Lipocalin-2, KIM-1, cystatin C, TIMP-1, β2M and OPN <em>via</em> Multiplex ELISAs. Albumin, and NGAL/lipocalin-2 were significantly elevated in the PAVP <em>vs</em> PS group on GD14 and GD18 (<em>p</em> < 0.001) respectively. VEGF-A significantly decreased in the pregnant <em>vs</em> non-pregnant groups on GD14 and 18 (<em>p</em> < 0.001). Clusterin (<em>p</em> < 0.001) and OPN (<em>p</em> < 0.05) were significantly higher in the PAVP <em>vs</em> PS group on GD18. Cystatin C and KIM-1 are significantly upregulated in the PAVP <em>vs</em> PS groups throughout gestation (<em>p</em> < 0.05). β2M is significantly elevated in the PAVP <em>vs</em> PS group on GD14 and 18 (<em>p</em> < 0.05). AVP elevated the urinary levels of the kidney injury biomarkers and replicated the renal dysfunction associated with PE development. Our findings confirm the potential applications of this model in studying the mechanisms underlying renal damage in PE.</p></div>","PeriodicalId":2,"journal":{"name":"ACS Applied Bio Materials","volume":null,"pages":null},"PeriodicalIF":4.6000,"publicationDate":"2024-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1642431X24000561/pdfft?md5=adfdaaf7b72132b24fa100705cd2a8b5&pid=1-s2.0-S1642431X24000561-main.pdf","citationCount":"0","resultStr":"{\"title\":\"Is renal dysfunction amplified in an arginine vasopressin induced rat model of preeclampsia?\",\"authors\":\"Sapna Ramdin , Thajasvarie Naicker , Sooraj Baijnath , Nalini Govender\",\"doi\":\"10.1016/j.repbio.2024.100910\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>Renal dysfunction is important in preeclampsia (PE) pathophysiology and has not been fully explored in the arginine vasopressin (AVP) rat model of PE. This study aimed to determine kidney toxicity associated with this model. Female Sprague Dawley rats (n = 24) were subcutaneously infused with AVP or saline for 18 days. Urine samples (GD8, 14 and 18) were used to determine the levels of albumin, VEGF-A, clusterin, NGAL/Lipocalin-2, KIM-1, cystatin C, TIMP-1, β2M and OPN <em>via</em> Multiplex ELISAs. Albumin, and NGAL/lipocalin-2 were significantly elevated in the PAVP <em>vs</em> PS group on GD14 and GD18 (<em>p</em> < 0.001) respectively. VEGF-A significantly decreased in the pregnant <em>vs</em> non-pregnant groups on GD14 and 18 (<em>p</em> < 0.001). Clusterin (<em>p</em> < 0.001) and OPN (<em>p</em> < 0.05) were significantly higher in the PAVP <em>vs</em> PS group on GD18. Cystatin C and KIM-1 are significantly upregulated in the PAVP <em>vs</em> PS groups throughout gestation (<em>p</em> < 0.05). β2M is significantly elevated in the PAVP <em>vs</em> PS group on GD14 and 18 (<em>p</em> < 0.05). AVP elevated the urinary levels of the kidney injury biomarkers and replicated the renal dysfunction associated with PE development. Our findings confirm the potential applications of this model in studying the mechanisms underlying renal damage in PE.</p></div>\",\"PeriodicalId\":2,\"journal\":{\"name\":\"ACS Applied Bio Materials\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":4.6000,\"publicationDate\":\"2024-06-07\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.sciencedirect.com/science/article/pii/S1642431X24000561/pdfft?md5=adfdaaf7b72132b24fa100705cd2a8b5&pid=1-s2.0-S1642431X24000561-main.pdf\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"ACS Applied Bio Materials\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1642431X24000561\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"MATERIALS SCIENCE, BIOMATERIALS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Bio Materials","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1642431X24000561","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MATERIALS SCIENCE, BIOMATERIALS","Score":null,"Total":0}
Is renal dysfunction amplified in an arginine vasopressin induced rat model of preeclampsia?
Renal dysfunction is important in preeclampsia (PE) pathophysiology and has not been fully explored in the arginine vasopressin (AVP) rat model of PE. This study aimed to determine kidney toxicity associated with this model. Female Sprague Dawley rats (n = 24) were subcutaneously infused with AVP or saline for 18 days. Urine samples (GD8, 14 and 18) were used to determine the levels of albumin, VEGF-A, clusterin, NGAL/Lipocalin-2, KIM-1, cystatin C, TIMP-1, β2M and OPN via Multiplex ELISAs. Albumin, and NGAL/lipocalin-2 were significantly elevated in the PAVP vs PS group on GD14 and GD18 (p < 0.001) respectively. VEGF-A significantly decreased in the pregnant vs non-pregnant groups on GD14 and 18 (p < 0.001). Clusterin (p < 0.001) and OPN (p < 0.05) were significantly higher in the PAVP vs PS group on GD18. Cystatin C and KIM-1 are significantly upregulated in the PAVP vs PS groups throughout gestation (p < 0.05). β2M is significantly elevated in the PAVP vs PS group on GD14 and 18 (p < 0.05). AVP elevated the urinary levels of the kidney injury biomarkers and replicated the renal dysfunction associated with PE development. Our findings confirm the potential applications of this model in studying the mechanisms underlying renal damage in PE.
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