Inflamação na doença renal crônica: papel de citocinas

Vianna, Heloísa Reniers; Soares, Cristina M. Bouissou; Tavares, Marcelo S; Teixeira, Mauro Martins; Silva, Ana Cristina Simões e

doi:10.1590/s0101-28002011000300012

Cited by 54 publications

(26 citation statements)

References 93 publications

(206 reference statements)

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“…There is also evidence of macrophage infiltration in the glomeruli of hypertensive animals [50] and humans [49]. Monocytes/macrophages in the kidney modulate blood pressure via the production of inflammatory cytokines and modulation of renin-angiotensin-aldosterone system [51, 52]. On the other hand, drugs acting on the renin-angiotensin-aldosterone system prevent or modulate inflammation [53].…”

Section: Relationship Between Monocytes/macrophages and Hypertensionmentioning

confidence: 99%

Pivotal Roles of Monocytes/Macrophages in Stroke

Chiba

Umegaki

2013

Mediators of Inflammation

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Stroke is an important issue in public health due to its high rates both of morbidity and mortality, and high rate of disability. Hypertension, cardiovascular disease, arterial fibrillation, diabetes mellitus, smoking, and alcohol abuse are all risk factors for stroke. Clinical observations suggest that inflammation is also a direct risk factor for stroke. Patients with stroke have high levels of inflammatory cytokines in plasma, and immune cells, such as macrophages and T-lymphocytes, are noted within stroke lesions. These inflammatory events are considered as a result of stroke. However, recent studies show that plasma levels of inflammatory cytokines or soluble adhesion molecules are high in patients without stroke, and anti-inflammatory therapy is effective at reducing stroke incidence in not only animal models, but in humans as well. Statins have been shown to decrease the stroke incidence via anti-inflammatory effects that are both dependent and independent of their cholesterol-lowering effects. These reports suggest that inflammation might directly affect the onset of stroke. Microglial cells and blood-derived monocytes/macrophages play important roles in inflammation in both onset and aggravation of stroke lesions. We review the recent findings regarding the role of monocytes/macrophages in stroke.

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Section: Relationship Between Monocytes/macrophages and Hypertensionmentioning

confidence: 99%

Pivotal Roles of Monocytes/Macrophages in Stroke

Chiba

Umegaki

2013

Mediators of Inflammation

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“…Chronic kidney disease is characterized by immunological and non-immunological injury of the glomerulus [12]. Previous studies have demonstrated an essential role of mesangial cells, specialized cells around blood vessels in the kidneys, in the immunological injury of the glomerulus [3].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of ERK1/2 by silymarin in mouse mesangial cells

Youn

Cho

Lee

et al. 2017

Korean J Physiol Pharmacol

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The present study aimed to show that pro-inflammatory cytokines [tumor necrosis factor (TNF)-α, interferon (IFN)-γ, and interleukin (IL)-1β] synergistically induce the production of nitric oxide (NO) production in mouse mesangial cells, which play an important role in inflammatory glomerular injury. We also found that co-treatment with cytokines at low doses (TNF-α; 5 ng/ml, IFN-γ; 5 ng/ml, and IL-1β; 1.25 U/ml) synergistically induced NO production, whereas treatment with each cytokine alone did not increase NO production at doses up to 100 ng/ml or 50 U/ml. Silymarin, a polyphenolic flavonoid isolated from milk thistle (Silybum marianum), attenuates cytokine mixture (TNF-α, IFN-γ, and IL-1β)-induced NO production. Western blot and RT-PCR analyses showed that silymarin inhibits inducible nitric oxide synthase (iNOS) expression in a dose-dependent manner. Silymarin also inhibited extracellular signal-regulated protein kinase-1 and -2 (ERK1/2) phosphorylation. Collectively, we have demonstrated that silymarin inhibits NO production in mouse mesangial cells, and may act as a useful anti-inflammatory agent.

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“…The development and progression of chronic kidney disease (CKD) is associated with inflammatory responses of various etiologies (1,2). Several previous studies have demonstrated that a variety of inflammatory mediators are involved in the pathophysiological processes of CKD (3,4).…”

Section: Introductionmentioning

confidence: 99%

Effects of dexamethasone on angiotensin II-induced changes of monolayer permeability and F-actin distribution in glomerular endothelial cells

Fang

Wang

Zhang

et al. 2013

Experimental and Therapeutic Medicine

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The aim of this study was to investigate the changes in monolayer permeability and F-actin distribution caused by angiotensin II (Ang II)-induced injury in glomerular endothelial cells (GENCs) and the effects of dexamethasone on these changes. GENCs isolated and cultured from Wistar rats were used to examine the changes in monolayer permeability and F-actin distribution induced by Ang II. GENC permeability was evaluated by measuring the diffusion of biotin-conjugated bovine serum albumin (biotin-BSA) across a cell monolayer. The expression levels and distribution of F-actin were assessed by flow cytometry. The biotin-BSA concentrations were measured by capture enzyme-linked immunosorbent assay. Ang II at a concentration of 10 mg/l increased the permeability of the GENC monolayer at 6 h and 12 h (P<0.05 and P<0.01, respectively) and caused F-actin depolymerisation at 6 h and 12 h (P<0.01). The two effects attributed to Ang II were significantly inhibited by dexamethasone treatment (P<0.01). The increased permeability of the GENC monolayer induced by Ang II was significantly correlated with the depolymerisation of F-actin. Dexamethasone abrogated the Ang II-mediated damage to GENCs indicating that it may play an important role in protecting GENCs from injury.

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Inflamação na doença renal crônica: papel de citocinas

Cited by 54 publications

References 93 publications

Pivotal Roles of Monocytes/Macrophages in Stroke

Pivotal Roles of Monocytes/Macrophages in Stroke

Inhibition of ERK1/2 by silymarin in mouse mesangial cells

Effects of dexamethasone on angiotensin II-induced changes of monolayer permeability and F-actin distribution in glomerular endothelial cells

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