Postnatal renin-angiotensin system inhibition prevents renal damage from prenatal inflammation in rats  

作　　者：Guo Wei Ji Yan Han Qi Yang Yao Wang Fangjie Yang Yongjian Deng Youcai Sun Xiongshan Li Xiaohui 

机构地区：[1]Institute of Materia Medica,College of Pharmacy and Department of Pharmacy,Southwest Hospital,Army Medical University(Third Military Medical University),Chongqing 400038,China [2]Department of Cardiology,The General Hospital of Western Theater Command(Chengdu Military General Hospital),Chengdu 610083,China

出　　处：《Journal of Traditional Chinese Medicine》2020年第4期646-653,共8页中医杂志（英文版）

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)。

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.

关 键 词：Renin-angiotensin system NF-kappa B BENAZEPRIL Prenatal inflammatory exposure 

分 类 号：R714.2[医药卫生—妇产科学] R692[医药卫生—临床医学]