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Signaling pathways modulated by fish oil in salt-sensitive hypertension. | LitMetric

Signaling pathways modulated by fish oil in salt-sensitive hypertension.

Am J Physiol Renal Physiol

Department of Laboratory Medicine and Pathology, Mayo Clinic College of Medicine, 200 First St. SW, Rochester, MN 55905, USA.

Published: June 2008

AI Article Synopsis

  • A study investigated how fish oil (FO) affects high blood pressure and kidney injury in Dahl salt-sensitive rats, finding significant reductions in blood pressure, protein in urine, and harmful kidney changes after 28 days on a diet high in FO.
  • FO also decreased levels of cholesterol, triglycerides, and interstitial inflammation in the kidneys, suggesting a protective effect.
  • The study proposes that FO's benefits are linked to its ability to inhibit certain cellular signaling pathways, including reduced activity of ERK, NF-kappaB, COX-2, and NADPH oxidase.

Article Abstract

Although many studies have indicated that fish oil (FO) improves cardiovascular risk factors and reduces histopathological manifestations of injury in experimental renal injury models, potential mechanisms underlying this protective effect have not been adequately defined. The objective of this study was to identify potential signaling pathways that confer protection in the Dahl rat model of salt-sensitive hypertension. Male Dahl salt-sensitive rats (n = 10/group) were provided with formulated diets containing 8% NaCl, 20% protein, and 25% FO or 25% corn oil (CO) for 28 days. FO reduced blood pressure (-11% at 4 wk; P < 0.05), urine protein excretion (-45% at 4 wk; P < 0.05), plasma cholesterol and triglyceride levels (-54%, P < 0.001; and -58%, P < 0.05), and histopathological manifestations of renal injury, including vascular hypertrophy, segmental and global glomerular sclerosis, interstitial fibrosis, and tubular atrophy. Interstitial inflammation was significantly reduced by FO (-32%; P < 0.001), as assessed by quantitative analysis of ED1-positive cells in sections of the renal cortex. FO reduced tubulointerstitial proliferative activity, as assessed by Western blot analysis of cortical homogenates for PCNA (-51%; P < 0.01) and quantitative analysis of Mib-1-stained sections of the renal cortex (-42%; P < 0.001). Decreased proliferative activity was associated with reduced phospho-ERK expression (-37%; P < 0.005) and NF-kappaB activation (-42%; P < 0.05). FO reduced cyclooxygenase (COX)-2 expression (-63%; P < 0.01) and membrane translocation of the NADPH oxidase subunits p47(phox) and p67(phox) (-26 and -34%; P < 0.05). We propose that FO ameliorates renal injury in Dahl salt-sensitive rats through the inhibition of ERK, decreased NF-kappaB activation, inhibition of COX-2 expression, and decreased NADPH oxidase activation.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2879056PMC
http://dx.doi.org/10.1152/ajprenal.00401.2007DOI Listing

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