Show simple item record

dc.contributor.authorWilson, Justin L.
dc.contributor.authorDuan, Rong
dc.contributor.authorEl-Marakby, Ahmed
dc.contributor.authorAlhashim, Abdulmohsin
dc.contributor.authorLee, Dexter L.
dc.date.accessioned2012-10-26T20:35:09Z
dc.date.available2012-10-26T20:35:09Z
dc.date.issued2012-07-16en_US
dc.identifier.citationPPAR Res. 2012 Jul 16; 2012:645969en_US
dc.identifier.issn1687-4765en_US
dc.identifier.pmid22848208en_US
dc.identifier.doi10.1155/2012/645969en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/815
dc.description.abstractThe anti-inflammatory properties of PPAR-α plays an important role in attenuating hypertension. The current study determines the anti-hypertensive and anti-inflammatory role of PPAR-α agonist during a slow-pressor dose of Ang II (400 ng/kg/min). Ten to twelve week old male PPAR-α KO mice and their WT controls were implanted with telemetry devices and infused with Ang II for 12 days. On day 12 of Ang II infusion, MAP was elevated in PPAR-α KO mice compared to WT (161 ± 4mmHg versus 145 ± 4 mmHg) and fenofibrate (145 mg/kg/day) reduced MAP in WT + Ang II mice (134 ± 7 mmHg). Plasma IL-6 levels were higher in PPAR-α KO mice on day 12 of Ang II infusion (30 ± 4 versus 8 ± 2 pg/mL) and fenofibrate reduced plasma IL-6 in Ang II-treatedWT mice (10±3 pg/mL). Fenofibrate increased renal expression of CYP4A, restored renal CYP2J expression, reduced the elevation in renal ICAM-1,MCP-1 and COX-2 inWT + Ang II mice. Our results demonstrate that activation of PPAR-α attenuates Ang II-induced hypertension through up-regulation of CYP4A and CYP2J and an attenuation of inflammatory markers such as plasma IL-6, renal MCP-1, renal expression of ICAM-1 and COX-2.
dc.rightsCopyright © 2012 Justin L. Wilson et al.en_US
dc.subjectResearch Articleen_US
dc.titlePeroxisome Proliferator Activated Receptor-α Agonist Slows the Progression of Hypertension, Attenuates Plasmaen_US
dc.typeArticleen_US
dc.identifier.pmcidPMC3405818en_US
dc.contributor.corporatenameDepartment of Oral Biology
dc.contributor.corporatenameDepartment of Pharmacology and Toxicology
refterms.dateFOA2019-04-10T00:56:58Z
html.description.abstractThe anti-inflammatory properties of PPAR-α plays an important role in attenuating hypertension. The current study determines the anti-hypertensive and anti-inflammatory role of PPAR-α agonist during a slow-pressor dose of Ang II (400 ng/kg/min). Ten to twelve week old male PPAR-α KO mice and their WT controls were implanted with telemetry devices and infused with Ang II for 12 days. On day 12 of Ang II infusion, MAP was elevated in PPAR-α KO mice compared to WT (161 ± 4mmHg versus 145 ± 4 mmHg) and fenofibrate (145 mg/kg/day) reduced MAP in WT + Ang II mice (134 ± 7 mmHg). Plasma IL-6 levels were higher in PPAR-α KO mice on day 12 of Ang II infusion (30 ± 4 versus 8 ± 2 pg/mL) and fenofibrate reduced plasma IL-6 in Ang II-treatedWT mice (10±3 pg/mL). Fenofibrate increased renal expression of CYP4A, restored renal CYP2J expression, reduced the elevation in renal ICAM-1,MCP-1 and COX-2 inWT + Ang II mice. Our results demonstrate that activation of PPAR-α attenuates Ang II-induced hypertension through up-regulation of CYP4A and CYP2J and an attenuation of inflammatory markers such as plasma IL-6, renal MCP-1, renal expression of ICAM-1 and COX-2.


Files in this item

Thumbnail
Name:
645969.pdf
Size:
851.8Kb
Format:
PDF

This item appears in the following Collection(s)

Show simple item record