Early postnatal treatment with soluble epoxide hydrolase inhibitor or 15-deoxy-Δ12,14-prostagandin J2 prevents prenatal dexamethasone and postnatal high saturated fat diet induced programmed hypertension in adult rat offspring

Pei Chen Lu, Jiunn Ming Sheen, Hong Ren Yu, Yu Ju Lin, Chih Cheng Chen, Mao Meng Tiao, Ching Chou Tsai, Li Tung Huang, You Lin Tain*

*此作品的通信作者

研究成果: 期刊稿件文章同行評審

11 引文 斯高帕斯(Scopus)

摘要

Prenatal dexamethasone (DEX) exposure, postnatal high-fat (HF) intake, and arachidonic acid pathway are closely related to hypertension. We tested whether a soluble epoxide hydrolase (SEH) inhibitor, 12-(3-adamantan-1-yl-ureido)-dodecanoic acid (AUDA) or 15-deoxy-Δ12,14-prostagandin J2 (15dPGJ2) therapy can rescue programmed hypertension in the DEX + HF two-hit model. Four groups of Sprague Dawley rats were studied: control, DEX + HF, AUDA, and 15dPGJ2. Dexamethasone (0.1 mg/kg body weight) was intraperitoneally administered to pregnant rats from gestational day 16-22. Male offspring received high-fat diet (D12331, Research Diets) from weaning to 4 months of age. In AUDA group, mother rats received 25 mg/L in drinking water during lactation. In the 15dPGJ2 group, male offspring received 15dPGJ2 1.5 mg/kg BW by subcutaneous injection once daily for 1 week after birth. We found postnatal HF diet aggravated prenatal DEX-induced programmed hypertension, which was similarly prevented by early treatment with AUDA or 15dPGJ2. The beneficial effects of AUDA and 15d-PGJ2 therapy include inhibition of SEH, increases of renal angiotensin converting enzyme-2 (ACE2) and angiotensin II type 2 receptor (AT2R) protein levels, and restoration of nitric oxide bioavailability. Better understanding of the impact of arachidonic acid pathway in the two-hit model will help prevent programmed hypertension in children exposed to corticosteroids and postnatal HF intake.

原文英語
頁(從 - 到)1-8
頁數8
期刊Prostaglandins and Other Lipid Mediators
124
DOIs
出版狀態已出版 - 01 07 2016

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© 2016 Elsevier Inc. All rights reserved.

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