15-Hydroxyprostaglandin dehydrogenase inhibitor prevents contrast-induced acute kidney injury

Autor: Ki Beom Bae, Dong-Hyun Kim, Sun Woo Kang, Byeong Woo Kim, Hye Jung Kim, Sanford D. Markowitz, Hyung Joo Baik, Mi Seon Kang, Sun-Hee Kim
Jazyk: angličtina
Rok vydání: 2021
Předmět:
medicine.medical_specialty
contrast media
acute kidney injury
Pyridines
media_common.quotation_subject
Prostaglandin E2
030232 urology & nephrology
Hemodynamics
Contrast Media
Thiophenes
030204 cardiovascular system & hematology
Critical Care and Intensive Care Medicine
Kidney
Iodinated contrast media
03 medical and health sciences
Mice
0302 clinical medicine
15 hydroxyprostaglandin dehydrogenase
Lipocalin-2
Internal medicine
Laboratory Study
Triiodobenzoic Acids
medicine
Contrast (vision)
Animals
Humans
media_common
urogenital system
business.industry
Prostaglandins E
Acute kidney injury
General Medicine
Acute Kidney Injury
medicine.disease
Diseases of the genitourinary system. Urology
15-PGDH inhibitor
Mice
Inbred C57BL
Endocrinology
Nephrology
Creatinine
Hydroxyprostaglandin Dehydrogenases
Female
RC870-923
medicine.symptom
business
Vasoconstriction
medicine.drug
Research Article
Zdroj: Renal Failure
article-version (VoR) Version of Record
Renal Failure, Vol 43, Iss 1, Pp 168-179 (2021)
ISSN: 1525-6049
0886-022X
Popis: The two primary mechanisms by which iodinated contrast media (CM) causes contrast-induced acute kidney injury (CIAKI) are the hemodynamic effect causing intrarenal vasoconstriction and the tubular toxic effect causing acute tubular necrosis. Inhibition of 15-hydroxyprostaglandin dehydrogenase (15-PGDH), which degrades prostaglandin E2 (PGE2), promotes tissue repair and regeneration in many organs. PGE2 causes intrarenal arterial vasodilation. In this study, we investigated whether a 15-PGDH inhibitor can act as a candidate for blocking these two major mechanisms of CIAKI. We established a CIAKI mouse model by injecting a 10 gram of iodine per body weight (gI/kg) dose of iodixanol into each mouse tail vein. A 15-PGDH inhibitor (SW033291), PGE1, or PGE2 were administered to compare the renal functional parameters, histologic injury, vasoconstriction, and renal blood flow changes. In addition, human renal proximal tubular epithelial cells were cultured in a CM-treated medium. SW033291, PGE1, or PGE2 were added to compare any changes in cell viability and apoptosis rate. CIAKI mice that received SW033291 had lower serum levels of creatinine, neutrophil gelatinase-associated lipocalin, and kidney injury molecule 1 (p
Databáze: OpenAIRE
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