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[PMID]:29267498
[Au] Autor:Ni XJ; Xu ZQ; Jin H; Zheng SL; Cai Y; Wang JJ
[Ad] Endereço:Transplantation Center, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
[Ti] Título:Ginsenoside Rg1 protects human renal tubular epithelial cells from lipopolysaccharide-induced apoptosis and inflammation damage.
[So] Source:Braz J Med Biol Res;51(2):e6611, 2017 Dec 11.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Ginsenoside Rg1, one of the most notable active components of Panax ginseng, has been widely reported to exert anti-inflammatory actions. This study aimed to reveal whether ginsenoside Rg1 also exhibits beneficial roles against lipopolysaccharide (LPS)-induced apoptosis and inflammation in human renal tubular epithelial cells, and to evaluate the potential role of the component on tubulointerstitial nephritis treatment. HK-2 cells were treated with various doses of ginsenoside Rg1 (0, 50, 100, 150, and 200 µM) in the absence or presence of 5 µg/mL LPS. Thereafter, CCK-8 assay, flow cytometry, western blot, migration assay, reactive oxygen species (ROS) assay, and ELISA were carried out to respectively assess cell viability, apoptosis, migration, ROS activity, and the release of inflammatory cytokines. As a result, ginsenoside Rg1 protected HK-2 cells from LPS-induced injury, as cell viability was increased, cell apoptosis was decreased, and the release of MCP-1, IL-1ß, IL-6, and TNF-α was reduced. Ginsenoside Rg1 functioned to HK-2 cells in a dose-dependent manner, and the 150 µM dose exhibited the most protective functions. Ginsenoside Rg1 had no significant impact on cell migration and ROS activity, while it alleviated LPS-induced ROS release and migration impairment. Furthermore, the down-regulations of p-PI3K, p-AKT, and up-regulations of PTEN, p-IκBα, p-p65, Bcl-3 induced by LPS were recovered to some extent after ginsenoside Rg1 treatment. In conclusion, ginsenoside Rg1 protects HK-2 cells against LPS-induced inflammation and apoptosis via activation of the PI3K/AKT pathway and suppression of NF-κB pathway.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Apoptose/efeitos dos fármacos
Células Epiteliais/efeitos dos fármacos
Ginsenosídeos/farmacologia
Túbulos Renais/citologia
Lipopolissacarídeos
Nefrite/prevenção & controle
[Mh] Termos MeSH secundário: Análise de Variância
Western Blotting
Linhagem Celular
Ensaios de Migração Celular
Sobrevivência Celular/efeitos dos fármacos
Citocinas/análise
Citocinas/efeitos dos fármacos
Ensaio de Imunoadsorção Enzimática
Seres Humanos
Túbulos Renais/efeitos dos fármacos
Fosfatidilinositol 3-Quinases/análise
Fosfatidilinositol 3-Quinases/efeitos dos fármacos
Substâncias Protetoras/farmacologia
Proteínas Proto-Oncogênicas c-akt/análise
Proteínas Proto-Oncogênicas c-akt/efeitos dos fármacos
Espécies Reativas de Oxigênio/análise
Reprodutibilidade dos Testes
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Cytokines); 0 (Ginsenosides); 0 (Lipopolysaccharides); 0 (Protective Agents); 0 (Reactive Oxygen Species); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); PJ788634QY (ginsenoside Rg1)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


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[PMID]:28469119
[Au] Autor:Okaka EI; Okwuonu CG
[Ad] Endereço:Department of Medicine, Renal Unit, University of Benin Teaching Hospital, University of Benin, Benin City, Nigeria.
[Ti] Título:Blood pressure variation and its correlates among patients undergoing hemodialysis for renal failure in Benin City, Nigeria.
[So] Source:Ann Afr Med;16(2):65-69, 2017 Apr-Jun.
[Is] ISSN:0975-5764
[Cp] País de publicação:India
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Blood pressure (BP) variation is commonly encountered during hemodialysis (HD) procedure. Both intradialysis hypotension and hypertension have implications for outcome of treatment and overall morbidity and mortality of the patients. METHODOLOGY: A retrospective study was carried out in the dialysis unit of a tertiary health institution in Benin City among patients who had HD for acute kidney injury (AKI) or chronic kidney disease (CKD) over a 3-year period. Data retrieved included age, gender, type of kidney disease, cause of kidney disease, systolic BP at onset of dialysis and at end of dialysis, and diastolic BP (DBP) at onset of and at end of dialysis. RESULTS: Complete data were available for 217 patients. One hundred and seven patients (49.3%) had no significant change in BP; 30.9% had intradialytic hypertension (IDHT) while 19.8% had intradialytic hypotension (IDH). IDH was more prevalent among patients with diabetic kidney disease while IDHT was more common among patients with hypertensive nephropathy (P = 0.002). Female patients had higher mean BP parameters compared to male patients pre- and post-dialysis, but only changes in DBP were statistically significant (P = 0.029). Patients with CKD had higher mean BP parameters pre- and post-dialysis compared to patients with acute AKI and the differences were statistically significant. CONCLUSION: Females had higher mean BP parameters than males. Patients with CKD had higher mean BP parameters compared with AKI patients. IDHT is a significant problem among patients on HD in our center. Measures to curtail this trend should be instituted with the goal of reducing morbidity and mortality.
[Mh] Termos MeSH primário: Lesão Renal Aguda/terapia
Pressão Sanguínea/fisiologia
Hipertensão Renal/terapia
Hipertensão/etiologia
Hipotensão/etiologia
Nefrite/terapia
Diálise Renal/efeitos adversos
[Mh] Termos MeSH secundário: Adulto
Idoso
Feminino
Unidades Hospitalares de Hemodiálise
Hospitais Universitários
Seres Humanos
Masculino
Meia-Idade
Nigéria/epidemiologia
Prevalência
Insuficiência Renal Crônica/complicações
Estudos Retrospectivos
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171211
[Lr] Data última revisão:
171211
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.4103/aam.aam_29_16


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[PMID]:28880939
[Au] Autor:Lin JS; Jeon JS; Fan Q; Wong HN; Palmer MB; Holzman LB
[Ad] Endereço:Division of Internal Medicine, Department of Emergency Medicine, Section of Nephrology, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America.
[Ti] Título:ARF6 mediates nephrin tyrosine phosphorylation-induced podocyte cellular dynamics.
[So] Source:PLoS One;12(9):e0184575, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:ADP-ribosylation factor 6 (ARF6) is a small GTPase necessary for regulating cellular structure, motility, and vesicle trafficking. In several cellular systems, ARF6 was shown to regulate actin dynamics in coordination with Rac1, a Rho small GTPase. We examined the function of ARF6 in the kidney podocyte because Rac1 was implicated in kidney diseases involving this cell. We found that ARF6 expression was enriched in human podocytes and that it modulated podocyte cytoskeletal dynamics through a functional interaction with nephrin, an intercellular junction protein necessary for podocyte injury-induced signaling requiring activation by tyrosine phosphorylation of its cytoplasmic domain. ARF6 was necessary for nephrin activation-induced ruffling and focal adhesion turnover, possibly by altering Rac1 activity. In podocyte-specific Arf6 (ARF6_PodKO) knockout mice, ARF6 deficiency did not result in a spontaneous kidney developmental phenotype or proteinuria after aging. However, ARF6_PodKO mice exhibited distinct phenotypes in two in vivo glomerular injury models. In the protamine sulfate perfusion model, which induced acute podocyte effacement, ARF6_PodKO mice were protected from podocyte effacement. In the nephrotoxic serum nephritis model, which induced immune-complex mediated injury, ARF6_PodKO mice exhibited aggravated proteinuria. Together, these observations suggest that while ARF6 is necessary for nephrin tyrosine phosphorylation-induced cytoskeletal dynamics in cultured podocytes, ARF6 has pleotropic podocyte roles in vivo, where glomerular injury-specific mechanisms might activate distinct signaling pathways that dictate whether ARF6 activity is beneficial or deleterious for maintaining the integrity of the glomerular filtration barrier.
[Mh] Termos MeSH primário: Fatores de Ribosilação do ADP/metabolismo
Nefrite/metabolismo
[Mh] Termos MeSH secundário: Fatores de Ribosilação do ADP/genética
Animais
Feminino
Seres Humanos
Rim/metabolismo
Rim/patologia
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Nefrite/genética
Podócitos/metabolismo
Receptores de IgG/genética
Receptores de IgG/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (Receptors, IgG); 0 (nephrin); EC 3.6.5.2 (ADP-Ribosylation Factors); EC 3.6.5.2 (ADP-ribosylation factor 6)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170908
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184575


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[PMID]:28873450
[Au] Autor:Yokota T; Omachi K; Suico MA; Kojima H; Kamura M; Teramoto K; Kaseda S; Kuwazuru J; Shuto T; Kai H
[Ad] Endereço:Department of Molecular Medicine, Graduate School of Pharmaceutical Sciences, Kumamoto University, 5-1 Oe-honmachi, Chuo-ku, Kumamoto City, Kumamoto, Japan.
[Ti] Título:Bromide supplementation exacerbated the renal dysfunction, injury and fibrosis in a mouse model of Alport syndrome.
[So] Source:PLoS One;12(9):e0183959, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A seminal study recently demonstrated that bromide (Br-) has a critical function in the assembly of type IV collagen in basement membrane (BM), and suggested that Br- supplementation has therapeutic potential for BM diseases. Because salts of bromide (KBr and NaBr) have been used as antiepileptic drugs for several decades, repositioning of Br- for BM diseases is probable. However, the effects of Br- on glomerular basement membrane (GBM) disease such as Alport syndrome (AS) and its impact on the kidney are still unknown. In this study, we administered daily for 16 weeks 75 mg/kg or 250 mg/kg (within clinical dosage) NaBr or NaCl (control) via drinking water to 6-week-old AS mice (mouse model of X-linked AS). Treatment with 75 mg/kg NaBr had no effect on AS progression. Surprisingly, compared with 250 mg/kg NaCl, 250 mg/kg NaBr exacerbated the progressive proteinuria and increased the serum creatinine and blood urea nitrogen in AS mice. Histological analysis revealed that glomerular injury, renal inflammation and fibrosis were exacerbated in mice treated with 250 mg/kg NaBr compared with NaCl. The expressions of renal injury markers (Lcn2, Lysozyme), matrix metalloproteinase (Mmp-12), pro-inflammatory cytokines (Il-6, Il-8, Tnf-α, Il-1ß) and pro-fibrotic genes (Tgf-ß, Col1a1, α-Sma) were also exacerbated by 250 mg/kg NaBr treatment. Notably, the exacerbating effects of Br- were not observed in wild-type mice. These findings suggest that Br- supplementation needs to be carefully evaluated for real positive health benefits and for the absence of adverse side effects especially in GBM diseases such as AS.
[Mh] Termos MeSH primário: Brometos/efeitos adversos
Nefropatias/metabolismo
Cirrose Hepática
Nefrite Hereditária/metabolismo
[Mh] Termos MeSH secundário: Animais
Nitrogênio da Ureia Sanguínea
Brometos/farmacologia
Creatinina/sangue
Modelos Animais de Doenças
Membrana Basal Glomerular/patologia
Rim/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Nefrite/patologia
Nitrogênio/sangue
Compostos de Potássio/efeitos adversos
Compostos de Potássio/farmacologia
Proteinúria/metabolismo
Compostos de Sódio/efeitos adversos
Compostos de Sódio/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bromides); 0 (Potassium Compounds); 0 (Sodium Compounds); AYI8EX34EU (Creatinine); LC1V549NOM (sodium bromide); N762921K75 (Nitrogen); OSD78555ZM (potassium bromide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171025
[Lr] Data última revisão:
171025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170906
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183959


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[PMID]:28808068
[Au] Autor:Liu Z; Huang XR; Chen HY; Fung E; Liu J; Lan HY
[Ad] Endereço:From the Division of Nephrology, the First Affiliated Hospital of Xinjiang Medical University, Urumqi, China (Z.L., J.L.); Department of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, Shatin, Hong Kong SAR, China (Z.L., X.-R.H., H.-Y.C., E.F., H.-Y.L.); and Shenzhen Research In
[Ti] Título:Deletion of Angiotensin-Converting Enzyme-2 Promotes Hypertensive Nephropathy by Targeting Smad7 for Ubiquitin Degradation.
[So] Source:Hypertension;70(4):822-830, 2017 Oct.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Angiotensin-converting enzyme-2 (ACE2) is downregulated in hypertensive nephropathy. The present study investigated the mechanisms whereby loss of ACE2 promoted angiotensin II-induced hypertensive nephropathy in ACE2 gene knockout mice. We found that compared with wild-type animals, mice lacking ACE2 developed much more severe hypertensive nephropathy in response to chronic angiotensin II infusion, including higher levels of blood pressure, urinary protein excretion, serum creatinine, and progressive renal fibrosis and inflammation. Mechanistic studies revealed that worsening kidney injury in ACE2 knockout mice was associated with an increase in Smurf2 (Smad-specific E3 ubiquitin protein ligase 2), a decrease in renal Smad7, and marked activation of TGF-ß (transforming growth factor ß)/Smad3 and NF-κB (nuclear factor κ-light-chain-enhancer of activated B cells) signaling, suggesting that Smurf2-dependent Smad7 ubiquitin degradation may be a key mechanism whereby loss of ACE2 promotes angiotensin II-induced TGF-ß/Smad3 and NF-κB-mediated hypertensive nephropathy. This was validated by restoring Smad7 locally in the kidneys of ACE2 knockout mice to block angiotensin II-induced TGF-ß/Smad3-mediated renal fibrosis and NF-κB-driven renal inflammation. Moreover, we found that angiotensin II could induce microRNA-21 in the mouse kidney and in cultured mesangial cells via a Smad3-dependent mechanism, which was enhanced by deleting ACE2 but inhibited by overexpressing renal Smad7. In conclusion, loss of ACE2 promotes angiotensin II-induced renal injury by targeting Smad7 for degradation via a Smurf2-dependent mechanism. Overexpression of renal Smad7 protects against hypertensive nephropathy by inactivating angiotensin II-induced TGF-ß/Smad3 and NF-κB pathways and by targeting the Smad3-dependent microRNA-21 axis.
[Mh] Termos MeSH primário: Pressão Sanguínea/fisiologia
Hipertensão Renal
Rim
Nefrite
Peptidil Dipeptidase A/metabolismo
Proteína Smad7/metabolismo
Ubiquitina/metabolismo
[Mh] Termos MeSH secundário: Animais
Regulação para Baixo/fisiologia
Fibrose/metabolismo
Hipertensão/metabolismo
Hipertensão Renal/metabolismo
Hipertensão Renal/patologia
Hipertensão Renal/fisiopatologia
Inflamação/metabolismo
Rim/metabolismo
Rim/patologia
Rim/fisiopatologia
Camundongos
Camundongos Knockout
NF-kappa B/metabolismo
Nefrite/metabolismo
Nefrite/patologia
Nefrite/fisiopatologia
Transdução de Sinais/fisiologia
Proteína Smad1/metabolismo
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-kappa B); 0 (Smad1 Protein); 0 (Smad1 protein, mouse); 0 (Smad7 Protein); 0 (Smad7 protein, mouse); 0 (Transforming Growth Factor beta); 0 (Ubiquitin); EC 3.4.15.1 (Peptidyl-Dipeptidase A); EC 3.4.17.- (angiotensin converting enzyme 2)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.117.09600


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[PMID]:28760771
[Au] Autor:Tesch GH
[Ad] Endereço:Department of Nephrology, Monash Health, Clayton, Victoria, Australia greg.tesch@monash.edu.
[Ti] Título:Diabetic nephropathy - is this an immune disorder?
[So] Source:Clin Sci (Lond);131(16):2183-2199, 2017 Aug 15.
[Is] ISSN:1470-8736
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Chronic diabetes is associated with metabolic and haemodynamic stresses which can facilitate modifications to DNA, proteins and lipids, induce cellular dysfunction and damage, and stimulate inflammatory and fibrotic responses which lead to various types of renal injury. Approximately 30-40% of patients with diabetes develop nephropathy and this renal injury normally progresses in about a third of patients. Due to the growing incidence of diabetes, diabetic nephropathy is now the main cause of end-stage renal disease (ESRD) worldwide. Accumulating evidence from experimental and clinical studies has demonstrated that renal inflammation plays a critical role in determining whether renal injury progresses during diabetes. However, the immune response associated with diabetic nephropathy is considerably different to that seen in autoimmune kidney diseases or in acute kidney injury arising from episodes of ischaemia or infection. This review evaluates the role of the immune system in the development of diabetic nephropathy, including the specific contributions of leucocyte subsets (macrophages, neutrophils, mast cells, T and B lymphocytes), danger-associated molecular patterns (DAMPs), inflammasomes, immunoglobulin and complement. It also examines factors which may influence the development of the immune response, including genetic factors and exposure to other kidney insults. In addition, this review discusses therapies which are currently under development for targeting the immune system in diabetic nephropathy and indicates those which have proceeded into clinical trials.
[Mh] Termos MeSH primário: Nefropatias Diabéticas/imunologia
Doenças do Sistema Imune/imunologia
[Mh] Termos MeSH secundário: Imunidade Adaptativa
Animais
Ativação do Complemento/imunologia
Nefropatias Diabéticas/etiologia
Nefropatias Diabéticas/genética
Modelos Animais de Doenças
Regulação da Expressão Gênica/imunologia
Seres Humanos
Doenças do Sistema Imune/etiologia
Doenças do Sistema Imune/genética
Imunidade Inata
Inflamação/complicações
Inflamação/genética
Inflamação/imunologia
Mediadores da Inflamação/metabolismo
Macrófagos/imunologia
Mastócitos/imunologia
Nefrite/complicações
Neutrófilos/imunologia
Receptores Imunológicos/metabolismo
Transdução de Sinais/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Inflammation Mediators); 0 (Receptors, Immunologic)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170802
[St] Status:MEDLINE
[do] DOI:10.1042/CS20160636


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[PMID]:28719617
[Au] Autor:Leiss H; Salzberger W; Jacobs B; Gessl I; Kozakowski N; Blüml S; Puchner A; Kiss A; Podesser BK; Smolen JS; Stummvoll GH
[Ad] Endereço:Department of Rheumatology, Medical University of Vienna, Vienna, Austria.
[Ti] Título:MicroRNA 155-deficiency leads to decreased autoantibody levels and reduced severity of nephritis and pneumonitis in pristane-induced lupus.
[So] Source:PLoS One;12(7):e0181015, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: We herein examine the role of endogenous miR155 in the development of systemic manifestations in pristane induced lupus. MATERIALS AND METHODS: Systemic lupus in miR155-deficient and wild type mice was induced upon injection of pristane and analyzed after 8 months, PBS-injected mice served as controls. Glomerulonephritis and pneumonitis were quantified using the kidney biopsy score and a newly adapted histomorphometric image analysis system; lung tissue was further analyzed by tissue cytometry. Serum levels of anti-dsDNA, anti-histone and anti-chromatin antibodies were measured by ELISA. Frequencies of B cells, activated and regulatory CD4+ T cells as well as Th1, Th2, Th17 cells were measured by flow cytometry. RT-qPCR was used to measure expression levels of interferon-signature and T-cell subset related as well as miR155-associated genes. RESULTS: After induction of lupus, miR155-deficient mice had significant less pulmonary involvement (perivascular inflammatory area in mm2/mm2 lung area 0.00092±0.00015 vs. 0.0027±0.00075, p = 0.0347) and renal disease (glomerular activity score 1.95±0.19 vs 3±0.26, p = 0.0029) compared to wild types. MiR155-deficient mice had significantly lower serum levels of disease-associated auto-antibodies and decreased frequencies of activated CD4+CD25+ (Foxp3-) cells. Upon restimulation, CD4+ cells showed a less pronounced Th2 and Th17 and a slightly decreased Th1 response in mir155-deficient mice. Pristane-treated wild types showed significantly up-regulated expression of genes related to the INF-signature (MX1, IP10, IRF7, ISG15). CONCLUSIONS: MiR155-deficient mice had less severe organ involvement, lower serum auto-antibody levels, a less prominent T cell response and lower expressions of genes jointly responsible for disease development. Thus, antagonizing miR155 might be a future approach in treating SLE.
[Mh] Termos MeSH primário: Autoanticorpos/metabolismo
Lúpus Eritematoso Sistêmico/complicações
MicroRNAs/metabolismo
Nefrite/tratamento farmacológico
Pneumonia/tratamento farmacológico
Terpenos/farmacologia
[Mh] Termos MeSH secundário: Animais
Regulação da Expressão Gênica/efeitos dos fármacos
Regulação da Expressão Gênica/imunologia
Interferons/metabolismo
Rim/efeitos dos fármacos
Rim/imunologia
Pulmão/efeitos dos fármacos
Pulmão/imunologia
Lúpus Eritematoso Sistêmico/induzido quimicamente
Camundongos
Nefrite/complicações
Nefrite/imunologia
Nefrite/metabolismo
Pneumonia/complicações
Pneumonia/imunologia
Pneumonia/metabolismo
Subpopulações de Linfócitos T/efeitos dos fármacos
Subpopulações de Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (MicroRNAs); 0 (Mirn155 microRNA, mouse); 0 (Terpenes); 26HZV48DT1 (pristane); 9008-11-1 (Interferons)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170719
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181015


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[PMID]:28665194
[Au] Autor:Özkök E; Yorulmaz H; Ates G; Aydin I; Ergüven M; Tamer S
[Ad] Endereço:1 Deparment of Neuroscience, The Institute of Experimental Medicine, Istanbul University , Istanbul, Turkey.
[Ti] Título:The impact of pretreatment with simvastatin on kidney tissue of rats with acute sepsis.
[So] Source:Physiol Int;104(2):158-170, 2017 Jun 01.
[Is] ISSN:2498-602X
[Cp] País de publicação:Hungary
[La] Idioma:eng
[Ab] Resumo:It has been reported that changes in cytokine levels affect mitochondrial functions, levels of hypoxia-inducible factor α (HIF-1α), and tissue damage during sepsis. We aimed to investigate the effects of simvastatin pretreatment on mitochondrial enzyme activities, and on levels of ghrelin, HIF-1α, and thiobarbituric acid reactive substances (TBARS) in kidney tissue during sepsis. Rats were separated into four groups, namely, control, lipopolysaccharides (LPS) (20 mg/kg), simvastatin (20 mg/kg), and simvastatin + LPS. We measured the levels of mitochondrial enzyme activities and TBARS in the kidney using spectrophotometry. The histological structure of the kidney sections was examined after staining with hematoxylin and eosin. Tumor necrosis factor α (TNF-α), IL-10, HIF-1α, and ghrelin immunoreactivity were examined using proper antibodies. In tissue, TNF-α (p < 0.01) and HIF-1α (p < 0.05) levels were increased in the simvastatin + LPS and LPS groups. TBARS levels were higher in the LPS group than in the other groups (p < 0.01), but they were similar in the simvastatin + LPS and control groups (p > 0.05). Ghrelin immunoreactivity was lower in the LPS group (p < 0.05) and higher in the simvastatin + LPS group than in the LPS group (p < 0.01). We observed tubular damage in the sections of the LPS group. There were no differences in mitochondrial enzyme activities between the groups (p > 0.05). We observed that pretreatment of simvastatin caused favorable changes on ghrelin and TBARS levels in rats with sepsis.
[Mh] Termos MeSH primário: Rim/metabolismo
Rim/patologia
Nefrite/metabolismo
Nefrite/prevenção & controle
Sepse/metabolismo
Sepse/prevenção & controle
Sinvastatina/administração & dosagem
[Mh] Termos MeSH secundário: Doença Aguda
Animais
Anti-Inflamatórios/administração & dosagem
Rim/efeitos dos fármacos
Masculino
Nefrite/patologia
Pré-Medicação/métodos
Ratos
Ratos Wistar
Sepse/patologia
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); AGG2FN16EV (Simvastatin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170701
[St] Status:MEDLINE
[do] DOI:10.1556/2060.104.2017.2.8


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[PMID]:28604827
[Au] Autor:Haase R; Potthoff SA; Meyer-Schwesinger C; Frosch C; Wiech T; Panzer U; Königshausen E; Stegbauer J; Sellin L; Rump LC; Quack I; Woznowski M
[Ad] Endereço:Department of Nephrology, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany.
[Ti] Título:A novel in vivo method to quantify slit diaphragm protein abundance in murine proteinuric kidney disease.
[So] Source:PLoS One;12(6):e0179217, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Injury of the glomerular filter causes proteinuria by disrupting the sensitive interplay of the glomerular protein network. To date, studies of the expression and trafficking of glomerular proteins have been mostly limited to in vitro or histologic studies. Here, we report a novel in vivo biotinylation assay that allows the quantification of surface expression of glomerular proteins in mice. Kidneys were perfused in situ with biotin before harvest. Afterwards glomeruli were isolated and lyzed. The protein of interest was separated by immunoprecipitation and the amount of surface-expressed protein was quantified by Western blot analysis with streptavidin staining. As proof-of-concept, we examined the presence of nephrin in the slit diaphragm in two well-established murine models of proteinuric kidney disease: nephrotoxic nephritis and adriamycin nephropathy. In proteinuric animals, significantly less nephrin was detected in the slit diaphragm. When proteinuria decreased once again during the course of disease, the amount of surface nephrin returned to the baseline. Our present results suggest that our assay is a valuable tool to study the glomerular filter in proteinuric kidney diseases. Note that the assay is not limited to proteins expressed in the slit diaphragm, and all surface proteins that are accessible to biotin perfusion and immunoprecipitation qualify for this analysis.
[Mh] Termos MeSH primário: Nefropatias/urina
Proteínas de Membrana/urina
Proteinúria/urina
[Mh] Termos MeSH secundário: Albuminúria
Animais
Modelos Animais de Doenças
Expressão Gênica
Nefropatias/genética
Nefropatias/patologia
Glomérulos Renais/metabolismo
Glomérulos Renais/patologia
Masculino
Proteínas de Membrana/genética
Camundongos
Nefrite/genética
Nefrite/patologia
Nefrite/urina
Proteinúria/genética
Proteinúria/patologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (nephrin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170613
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179217


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[PMID]:28591051
[Au] Autor:Xu H; Li W; Mao JH; Pan YX
[Ad] Endereço:aDepartment of Clinical Laboratory bDepartment of Nephrology, Children's Hospital of Zhejiang University School of Medicine, Hangzhou, People's Republic of China.
[Ti] Título:Association between red blood cell distribution width and Henoch-Schonlein purpura nephritis.
[So] Source:Medicine (Baltimore);96(23):e7091, 2017 Jun.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:To investigate whether red blood cell distribution width (RDW) is a marker of the risk of Henoch-Schonlein purpura (HSP) nephritis (HSPN), a total of 669 HSP patients and 168 healthy controls were included in this retrospective study. Two hundred fifty-six (38.3%) of the patients had kidney involvement. Compared with the HSP group, RDW was significantly higher in the HSPN group (P < .001). Binary logistic regression identified that HSPN was independently associated with age, RDW, platelet, and total cholesterol (odds ratio = 1.409, 1.353, 0.996, and 2.019, respectively). In addition, RDW values of HSPN patients with crescents on histopathology (classes III, IV, and V) were higher compared with those of HSPN without crescents (classes I and II) (P = .019). The receiver-operating characteristic curve analysis showed that the RDW at a cut-off point of 13.25 has 61% sensitivity and 79% specificity in predicting the presence of crescents on histopathology. It was first shown that RDW levels in HSPN are significantly higher than those in HSP without nephritis and healthy controls. RDW can be an independent predictor of HSPN and its levels greater than 13.25 were useful in the predicting the presence of crescents on histopathology.
[Mh] Termos MeSH primário: Índices de Eritrócitos
Nefrite/sangue
Púrpura de Schoenlein-Henoch/sangue
[Mh] Termos MeSH secundário: Fatores Etários
Biomarcadores/sangue
Criança
Colesterol/sangue
Eritrócitos/patologia
Feminino
Seres Humanos
Modelos Logísticos
Masculino
Análise Multivariada
Razão de Chances
Prognóstico
Curva ROC
Estudos Retrospectivos
Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Biomarkers); 97C5T2UQ7J (Cholesterol)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170706
[Lr] Data última revisão:
170706
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170608
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000007091



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