Exacerbation of acute kidney injury by bone marrow stromal cells from rats with persistent renin-angiotensin system activation.

Hypertension and persistent activation of the renin-angiotensin system (RAS) are predisposing factors for the development of acute kidney injury (AKI). Although bone-marrow-derived stromal cells (BMSCs) have shown therapeutic promise in treatment of AKI, the impact of pathological RAS on BMSC functionality has remained unresolved. RAS and its local components in the bone marrow are involved in several key steps of cell maturation processes.

Dexmedetomidine preconditioning ameliorates kidney ischemia-reperfusion injury.

Kidney ischemia-reperfusion (I/R) injury is a common cause of acute kidney injury. We tested whether dexmedetomidine (Dex), an alpha2 adrenoceptor (α2-AR) agonist, protects against kidney I/R injury. Sprague-Dawley rats were divided into four groups: (1) Sham-operated group; (2) I/R group (40 min ischemia followed by 24 h reperfusion); (3) I/R group + Dex (1 μg/kg i.

Skeletal muscle gene expression profile is modified by dietary protein source and calcium during energy restriction.

Background/aims: The potential of whey protein and calcium to modify skeletal muscle gene expression during energy restriction (ER) was investigated in a model of diet-induced obesity.

Methods: Obese C57BL/6J mice received casein (calcium 0.4%) and two different high-calcium (1.

Effects of high-calcium diets with different whey proteins on weight loss and weight regain in high-fat-fed C57BL/6J mice.

The aim of the study was to compare the effect of different whey protein-containing high-Ca diets on weight loss and weight regain in a model of diet-induced obesity. Obesity was induced in C57BL/6J mice with a high-fat (60 % of energy) diet. Weight loss by energy restriction was performed on four different high-Ca diets (1.

Rosuvastatin protects against angiotensin II-induced renal injury in a dose-dependent fashion.

Objective: We showed earlier that statin treatment ameliorates target-organ injury in a transgenic model of angiotensin (Ang) II-induced hypertension. We now test the hypothesis that rosuvastatin (1, 10, and 50 mg/kg/day) influences leukocyte adhesion and infiltration, prevents induction of inducible nitric oxide synthase (iNOS), and ameliorates target-organ damage in a dose-dependent fashion.

Methods: We treated rats harboring the human renin and human angiotensinogen genes (dTGR) from week 4 to 8 (n = 20 per group).

Metabolomic changes in fatty liver can be modified by dietary protein and calcium during energy restriction.

Aim: To characterise the effect of energy restriction (ER) on liver lipid and primary metabolite profile by using metabolomic approach. We also investigated whether the effect of energy restriction can be further enhanced by modification of dietary protein source and calcium.

Methods: Liver metabolomic profile of lean and obese C57Bl/6J mice (n = 10/group) were compared with two groups of weight-reduced mice.

Effect of dietary calcium and dairy proteins on the adipose tissue gene expression profile in diet-induced obesity.

Background/aims: Calcium and dairy proteins have been postulated to explain why the intake of dairy products correlates inversely with body mass index in several populations. We have shown that a high-calcium diet with whey protein attenuates weight gain and now we describe the effects of this diet on adipose tissue gene expression.

Methods: Nine-week-old C57Bl/6J mice were divided into two groups (n = 10/group).

High-calcium diet with whey protein attenuates body-weight gain in high-fat-fed C57Bl/6J mice.

An inverse relationship between Ca intake and BMI has been found in several studies. It has been suggested that Ca affects adipocyte metabolism via suppressing 1,25-dihydroxycholecalciferol (1,25(OH)2-D3) and decreases fat absorption. We studied the effect of Ca and milk proteins (whey and casein) on body weight in C57Bl/6J mice.

Lipoic acid supplementation prevents cyclosporine-induced hypertension and nephrotoxicity in spontaneously hypertensive rats.

Background: Cyclosporine (CsA) has significantly improved long-term survival after organ transplantations. Hypertension and nephrotoxicity are common side effects during CsA treatment and are aggravated by high salt intake.

Objective: To examine whether lipoic acid (LA), a natural antioxidant that scavenges reactive oxygen species and regenerates/recycles endogenous antioxidants, could prevent CsA-induced hypertension and nephrotoxicity.

High sodium intake increases vascular superoxide formation and promotes atherosclerosis in apolipoprotein E-deficient mice.

Hypertension is a major risk factor for atherosclerosis. We tested the hypothesis whether high salt intake aggravates endothelial dysfunction and promotes atherosclerosis in apolipoprotein E-deficient mice (ApoE(-)/(-) mice) and their littermate controls (C57Bl/6 mice). The role of increased oxidative stress was also examined.

GSK-3beta inhibitors attenuate the organ injury/dysfunction caused by endotoxemia in the rat.

Objective: Serine-threonine protein kinase glycogen synthase kinase (GSK)-3 is involved in regulation of many cell functions, but its role in regulation of inflammatory response is unknown. Here we investigate the effects of GSK-3beta inhibition on organ injury/dysfunction caused by lipopolysaccharide or coadministration of lipopolysaccharide and peptidoglycan in the rat.

Design: Prospective, randomized study.

Magnesium supplementation prevents angiotensin II-induced myocardial damage and CTGF overexpression.

Objectives And Design: Magnesium deficiency promotes vasoconstriction and myocardial damage. Recent studies provide evidence that Ang II mobilizes intracellular Mg through AT1 receptor-mediated pathways. We tested the hypothesis of whether magnesium supplementation prevents Ang II-induced myocardial damage and induction of the profibrotic connective tissue growth factor (CTGF).

Resistance to salt-induced hypertension in catechol-O-methyltransferase-gene-disrupted mice.

Background: Previous studies have indicated that catechol-O-methyltransferase (COMT) can modulate renal dopaminergic tone.

Objective: To test the hypothesis that COMT blockade protects from salt-induced hypertension.

Methods: COMT gene-disrupted (-/-) mice and wild-type controls received a high-sodium diet (NaCl 6%) for 3 weeks.

Entacapone protects from angiotensin II-induced inflammation and renal injury.

Objectives And Design: Angiotensin II (Ang II)-induced renal damage is associated with perivascular inflammation and increased oxidative stress. We tested the hypothesis whether entacapone, a catechol-O-methyltransferase (COMT) inhibitor exerting antioxidative and anti-inflammatory properties, protects against the Ang II-induced inflammatory response and end-organ damage.

Methods: Samples from double-transgenic rats harbouring human renin and human angiotensinogen genes (dTGR) and normotensive Sprague-Dawley rats (SD) were assessed by light microscopy, immunohistochemistry, reverse transcriptase-polymerase chain reaction (RT-PCR), and high pressure liquid chromatography.

Cardiovascular and renal effects of cyclooxygenase inhibition in transgenic rats harboring mouse renin-2 gene (TGR[mREN2]27).

The present study examined the role of cyclooxygenase-synthetized prostanoids in the pathogenesis of angiotensin-II-induced inflammatory response and vascular injury in transgenic rats harboring mouse renin-2 gene (mREN2 rats). Five- to six-week-old, heterozygous mREN2 rats received the following drug regimens for 8 weeks: (1) controls; (2) cyclooxygenase-2 inhibitor (MF-tricyclic [3-(3,4-difluorophenyl)-4-(4-(methylsulfonyl) phenyl)-2(5H)-furanone], 14 mg kg(-1) p.o.

Lacidipine inhibits adhesion molecule and oxidase expression independent of blood pressure reduction in angiotensin-induced vascular injury.

Dihydropyridines can inhibit gene expression in-vitro and may have a protective vascular effect independent of blood pressure reduction. We tested the hypothesis that lacidipine prevents induction of inducible NO synthase (iNOS), influences leukocyte adhesion and infiltration, inhibits nuclear factor (NF)-kappaB transcription factor activity, and ameliorates end-organ damage in a transgenic rat model of angiotensin (Ang) II--dependent organ sclerosis. We treated rats transgenic for human renin and angiotensinogen (dTGR) from week 4 to 7 with lacidipine (0.