Paricalcitol prevents MAPK pathway activation and inflammation in adriamycin-induced kidney injury in rats.

Background: Activation of the mitogen-activated protein kinase (MAPK) pathway induces uncontrolled cell proliferation in response to inflammatory stimuli. Adriamycin (ADR)-induced nephropathy (ADRN) in rats triggers MAPK activation and pro-inflammatory mechanisms by increasing cytokine secretion, similar to chronic kidney disease (CKD). Activation of the vitamin D receptor (VDR) plays a crucial role in suppressing the expression of inflammatory markers in the kidney and may contribute to reducing cellular proliferation.

Paricalcitol Improves the Angiopoietin/Tie-2 and VEGF/VEGFR2 Signaling Pathways in Adriamycin-Induced Nephropathy.

Renal endothelial cell (EC) injury and microvascular dysfunction contribute to chronic kidney disease (CKD). In recent years, increasing evidence has suggested that EC undergoes an endothelial-to-mesenchymal transition (EndoMT), which might promote fibrosis. Adriamycin (ADR) induces glomerular endothelial dysfunction, which leads to progressive proteinuria in rodents.

Imbalance of Pro- and Anti-Angiogenic Factors Due to Maternal Vitamin D Deficiency Causes Renal Microvasculature Alterations Affecting the Adult Kidney Function.

Vitamin D (Vit.D) is involved in cellular proliferation and differentiation and regulation of the renin gene, which are important aspects of nephrogenesis and quiescence of renal health in adulthood. This study evaluated the angiogenic mechanisms involved in long term renal disturbances induced by Vit.

Protective effect of calcitriol on rhabdomyolysis-induced acute kidney injury in rats.

Glycerol injection in rats can lead to rhabdomyolysis, with the release of the intracellular muscle content to the extracellular compartment and acute kidney injury (AKI). Oxidative stress and the inflammatory processes contribute to the disturbances in renal function and structure observed in this model. This study evaluated the effect of calcitriol administration in AKI induced by rhabdomyolysis and its relationship with oxidative damage and inflammatory process.

Calcitriol reduces kidney development disorders in rats provoked by losartan administration during lactation.

Calcitriol has important effects on cellular differentiation and proliferation, as well as on the regulation of the renin gene. Disturbances in renal development can be observed in rats exposed to angiotensin II (AngII) antagonists during lactation period. The lack of tubular differentiation in losartan-treated rats can affect calcitriol uptake.

The role of oxidative stress in renal injury induced in rats by losartan exposure during lactation.

Introduction: Rats exposed to angiotensin II (AII) receptor antagonists during lactation present progressive disturbances in renal development that lead to progressive alterations in renal function and structure. This study evaluates the role of oxidative stress in the renal changes induced by exposure to losartan, a type 1 AII receptor antagonist, in rats during lactation.

Materials And Methods: Male Wistar pups were divided into: Control, pups of dams that received 2% sucrose solution; Control-tempol, pups of dams that received tempol (0.

Postnatal renal abnormalities in rats exposed to losartan during lactation.

Background/aims: Rats exposed to losartan during lactation exhibit progressive changes in renal function and structure. This study analyzed the early events in pups from dams that received losartan during lactation.

Methods: Male Wistar rats from dams that received 2% sucrose (control, n = 25) or losartan (100 mg/kg/day) diluted in 2% sucrose (n = 33) during lactation were anesthetized 21 days after birth.

Role of endogenous hydrogen sulfide on renal damage induced by adriamycin injection.

A single injection of adriamycin (ADR) induces marked and persistent proteinuria in rats that progress to glomerular and tubulointerstitial lesions. It has been shown that ADR-induced nephrotoxicity is mediated, at least in part, by oxidative stress that lead to inflammation. Endogenous hydrogen sulfide (H₂S) is synthesized from L-cysteine and is an important signaling molecule in inflammation.

Inhibition of hydrogen sulphide formation reduces cisplatin-induced renal damage.

Background: Cisplatin (CP)-induced renal damage is associated with inflammation. Hydrogen sulphide (H2S) is involved in models of inflammation. This study evaluates the effect of DL-propargylglycine (PAG), an inhibitor of endogenous H2S formation, on the renal damage induced by CP.

Renal structure and function evaluation of rats from dams that received increased sodium intake during pregnancy and lactation submitted or not to 5/6 nephrectomy.

Adult rats submitted to perinatal salt overload presented renin-angiotensin system (RAS) functional disturbances. The RAS contributes to the renal development and renal damage in a 5/6 nephrectomy model. The aim of the present study was to analyze the renal structure and function of offspring from dams that received a high-salt intake during pregnancy and lactation.

MAPK and angiotensin II receptor in kidney of newborn rats from losartan-treated dams.

Several lines of evidence suggest that angiotensin II (A-II) participates in the postnatal development of the kidney in rats. Many effects of A-II are mediated by mitogen-activated protein kinase (MAPK) pathways. This study investigated the influence that treatment with losartan during lactation has on MAPKs and on A-II receptor types 1 (AT(1)) and 2 (AT(2)) expression in the renal cortices of the offspring of dams exposed to losartan during lactation.

Resveratrol attenuates cisplatin-induced nephrotoxicity in rats.

Cisplatin is an antitumor drug widely used in the treatment of many malignant tumors. However, the most common adverse effect, nephrotoxicity, limits the use of this drug in many cancer patients. Resveratrol is a phytoalexin that presents highly efficient protection in experimental nephrotoxicity models.

The effects of oral glutamine on cisplatin-induced nephrotoxicity in rats.

The antioxidant activity of the amino acid glutamine was investigated to obtain protection against peroxidative damage in rat kidney and nephrotoxicity induced by the treatment with a single dose of the antitumoral cisplatin (5mgkg(-1) body weight). The animals were divided into four treatment and control groups of six rats each (n=6). Cisplatin was injected i.

The effects of oral glutamine on cisplatin-induced genotoxicity in Wistar rat bone marrow cells.

Several studies have suggested that dietary supplementation with antioxidants can influence the response to chemotherapy as well as the development of adverse side effects that result from treatment with antineoplastic agents. The emphasis of the present study was to investigate whether the administration of a single dose of oral glutamine had any protective effect against cisplatin-induced clastogenicity. Cisplatin was administered to Wistar rats either alone or after treatment with glutamine.