摘要
OBJECTIVE:To assess the protective role of benazepril,an angiotensin-converting enzyme inhibitor,in renal damage caused by prenatal inflammation.METHODS:Saline or lipopolysaccharide were administered intraperitoneally to pregnant Sprague-Dawley rats on gestation days 8,10,and 12.After birth,offspring received either tap water or benazepril in water between 7 and 68 weeks.Blood pressure,blood urea nitrogen,creatinine,and 24-h urine volume were measured as indices of renal function.Hematoxylin,eosin,periodic acid-Schiff,and Sirius Red staining were used to evaluate renal damage.RESULTS:Postnatal benazepril treatment ameliorated hypertension and restored normal 24-h urine volume and blood urea nitrogen and serum creatinine levels.Benazepril treatment also reduced glycoprotein accumulation and fibrosis in the glomerulus and in tubular epithelial cells and inhibited nuclear factor-kappa B activation.CONCLUSION:Together with our previous findings that postnatal inhibition of nuclear factor-kappa B activation blocks intra-renal renin-angiotensin system activation,our current data demonstrate that intra-renal activation of the renin-angiotensin system interacts with nuclear factor-kappa B activation to cause renal damage in adulthood following prenatal inflammation.
基金
Natural Science Foundation-funded Project:Role of HMGB-1-TLR4/RAGE Pathway Over-Expression in Increased Offspring's Pyelonephritis Sensitivity Induced by Pregnant Inflammatory Stimulation(No.81703522)
the Role and Mechanisms of Decidual NK Cell Abnormality in Prenatal Inflammation-Induced Offspring's Immune System Dysfunction and Hypertension(No.81520108029)
Role of AMPK/NK-ΚB Signal Pathway Imbalance in Offspring's Hypertension Induced by Pregnant Inflammatory Stimulation(No.81703521)
Roles and Mechanisms of Mitochondrial Dyshomeostasis in the Hypersensitivity of Cardiac Damage Responding to Cardiac Risk Factors in Offspring of Prenatal Inflammatory Stimulation(No.81773742)。
