Database : MEDLINE
Search on : kidney and cortex and necrosis [Words]
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[PMID]: 29430921
[Au] Autor:Zhao C; Xie P; Yong T; Wang H; Chung ACK; Cai Z
[Ad] Address:State Key Laboratory of Environmental and Biological Analysis, Department of Chemistry , Hong Kong Baptist University , Hong Kong SAR , P. R. China.
[Ti] Title:MALDI-MS Imaging Reveals Asymmetric Spatial Distribution of Lipid Metabolites from Bisphenol S-Induced Nephrotoxicity.
[So] Source:Anal Chem;90(5):3196-3204, 2018 Mar 06.
[Is] ISSN:1520-6882
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:With the continuous exposure of environmental pollutants in organisms, determination of abundance variation and spatial distribution of lipids might expand our understanding of toxicological mechanisms occurring in the kidney. Herein, an integrated method involving mass spectrometry (MS)-based lipidomics and matrix-assisted laser desorption/ionization-MS imaging (MALDI-MSI) was developed for the study of nephrotoxicity in mice exposed to 10 and 100 µg bisphenol S (BPS)/kg body weight/day. The BPS exposure remarkable perturbed abundances of 91 potential markers that mainly involved in five metabolic pathways. We elucidated the lipids spatial heterogeneity by using morphological analysis, probabilistic latent semantic analysis, and coregistered multimodal three-dimensional (3D)-MSI. In morphological analysis, both 10 and 100 µg BPS induced significant nephrotoxicity to mice, including glomerular necrosis in renal cortex, cloudy swelling in renal medulla, and interstitial collapsing in renal pelvis. Significant differential signaling lipids such as sphingomyelin (SM) (d22:0/20:4), ceramide (Cer) (d18:2/24:1), and sphingosine (d18:0) related to inflammation were found to be up-regulated and colocalized in the renal cortex, medulla, and pelvis, respectively. Also, seven significant differential lipids, which are considered to be involved in membrane homeostasis and cellular function, were found to be colocalized in the renal cortex. The observed significant variations of morphology, lipid accumulation, and metabolism in the renal cortex implicated that lipids in the renal cortex were more sensitive to BPS exposure than those in the renal medulla and pelvis. Moreover, we reconstructed a 3D-MSI model of kidney and identified two heterogeneous-related substructures in the renal cortex and pelvis upon 100 µg BPS exposure. It might be used in novel specificity evaluation and early diagnosis for environmental pollutant-induced kidney diseases.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:In-Data-Review
[do] DOI:10.1021/acs.analchem.7b04540

  2 / 1757 MEDLINE  
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[PMID]: 29409856
[Au] Autor:Abou-Hany HO; Atef H; Said E; Elkashef HA; Salem HA
[Ad] Address:Department of Pharmacology and Biochemistry, Faculty of Pharmacy, Delta University for Sciences and Technology, Gamasa, Egypt.
[Ti] Title:Crocin mediated amelioration of oxidative burden and inflammatory cascade suppresses diabetic nephropathy progression in diabetic rats.
[So] Source:Chem Biol Interact;284:90-100, 2018 Feb 03.
[Is] ISSN:1872-7786
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:Diabetic Nephropathy (DN) is one of the main complications associated with diabetes mellitus. Persistently elevated blood glucose level drives histopathological changes in renal tissues that hinder normal kidney functions. In the current study, crocin; the main bioactive constituent of Crocus sativus was investigated as a reno-protective agent against DN by virtue of its numerous pharmacological activities. Diabetes was induced in male Sprague-Dawely rats through intravenous injection of streptozocin (STZ) (50 mg/kg), DN was confirmed eight weeks post diabetes induction. Daily oral crocin for eight weeks (20 mg/kg) significantly reduced blood glucose level with a significant increase in insulin level. Moreover, crocin improved impaired kidney functions as manifested in reduction of serum creatinine levels, blood urea nitrogen and proteinuria with concomitant increase in urinary creatinine clearance. Furthermore, biomarkers of cell injury and tissue necrosis like LDH activity was significantly reduced, kidney content of NOS significantly declined likewise. In addition, renal antioxidants such as SOD, GSH and serum catalase activity significantly increased with concomitant reduction of kidney MDA; biomarker of oxidative load. Kidney content of toll-like receptors 4 and IL-6 significantly declined with simultaneous suppression of nuclear factor kappa-B (NF-κB/p65) protein expression and immuno-staining in rat renal cortex. Furthermore, crocin inhibited progression of renal fibrosis as seen with reduction of renal hydroxyproline and collagen content, TGF-ß immuno-staining and Masson's Trichrome positive tissue. Histopathologically, crocin pretreatment was associated with minimal renal damage with fewer fibrotic lesions. There was a concomitant restoration of renal tubules integrity with preservation of glomerular space area. In conclusion, crocin's ameliorative impact on DN may be attributed to its free radicals scavenging properties, its ability to enhance host antioxidant defense system and its ability to inhibit inflammatory and fibrotic cascades activation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[St] Status:Publisher

  3 / 1757 MEDLINE  
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[PMID]: 29319433
[Au] Autor:Fuentes-Delgado VH; Martínez-Saldaña MC; Rodríguez-Vázquez ML; Reyes-Romero MA; Reyes-Sánchez JL; Jaramillo-Juárez F
[Ad] Address:a Centro de Ciencias Básicas, Departamento de Fisiología y Farmacología , Universidad Autónoma de Aguascalientes , Aguascalientes , México.
[Ti] Title:Renal damage induced by the pesticide methyl parathion in male Wistar rats.
[So] Source:J Toxicol Environ Health A;81(6):130-141, 2018.
[Is] ISSN:1528-7394
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Little information is apparently available regarding the nephrotoxic effects induced by pesticides. The aim of this study was to examine the influence of low doses of methyl parathion (MP) on the structure and function of the kidney of male Wistar rats. A corn oil (vehicle) was administered to control rats, whereas treated rats received MP at 0.56 mg/kg orally (1/25 of LD ), every third day, for 8 weeks. At the end of each week following MP exposure, creatinine and glucose levels were measured in plasma, while glucose, inorganic phosphate, total proteins, albumin, and activity of γ-glutamyltranspeptidase (GGT) were determined in urine. Kidney histological study was also performed. Compared with control rats, MP significantly increased plasma glucose and creatinine levels accompanied by decreased urinary flow rate and elevated urinary excretion rates of glucose, phosphate, and albumin. Further, the activity of GGT in urine was increased significantly. The proximal cells exhibited cytoplasmic vacuolization, positive periodic acid Schiff inclusions, and brush border edge loss after 2 or 4 weeks following MP treatment. Finally, renal cortex samples were obtained at 2, 4, 6, and 8 weeks of MP treatment, and the concentrations of reduced glutathione (GSH) and glutathione peroxidase (GPx) activity were measured. The mRNA expression levels of BAX and tumor necrosis factor-α (TNF-α) were also determined (RT-PCR). MP significantly decreased renal GSH levels, increased GPx activity, as well as downregulated the mRNA expression of TNF-α and BAX. Densitometry analysis showed a significant reduction in TNF-α and BAX mRNA expression levels at 2 and 4 weeks following MP treatment. Low doses of MP produced structural and functional damage to the proximal tubules of male rat kidney.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180201
[Lr] Last revision date:180201
[St] Status:In-Data-Review
[do] DOI:10.1080/15287394.2017.1394948

  4 / 1757 MEDLINE  
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[PMID]: 29310372
[Au] Autor:Kim CS; Kim SS; Bae EH; Ma SK; Kim SW
[Ad] Address:Department of Internal Medicine.
[Ti] Title:Acute kidney injury due to povidone-iodine ingestion: A case report.
[So] Source:Medicine (Baltimore);96(48):e8879, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:RATIONALE: Povidone-iodine is a broad-spectrum antiseptic applied topically to treat wounds and prevent their infection. There have been several case reports of acute kidney injury (AKI) in burn patients after povidone-iodine irrigation and in patients receiving the substance as a sclerotherapy agent for management of lymphocele after renal transplantation. However, biopsy-confirmed AKI after ingestion of povidone-iodine has not previously been described. PATIENT CONCERNS: A 47-year-old man who had apparently ingested povidone-iodine solution and presented with nausea, vomiting, and reduced urine output. Laboratory data revealed blood urea nitrogen of 124 mg/dL, serum creatinine of 6.3 mg/dL, impaired liver function, and leukocytosis. Urine iodine/creatinine ratio was markedly elevated. DIAGNOSES: Acute tubular necrosis and interstitial nephritis secondary to povidone-iodine ingestion. INTERVENTIONS: The patient was admitted to the intensive care unit and underwent continuous venovenous hemodiafiltration. Kidney biopsy showed acute tubular necrosis and interstitial nephritis. Unstained sections showed tan objects in the tubular lumina that were suspected to be povidone-iodine casts. Corticosteroid therapy (1 mg/kg/day) was started after kidney biopsy. OUTCOMES: Renal function recovered after hemodialysis and corticosteroid medication, but not completely. LESSONS: We have reported the first case of biopsy-confirmed AKI accompanied by increased urine iodine concentration following povidone-iodine ingestion.
[Mh] MeSH terms primary: Acute Kidney Injury/chemically induced
Anti-Infective Agents, Local/poisoning
Povidone-Iodine/poisoning
[Mh] MeSH terms secundary: Acute Kidney Injury/therapy
Adrenal Cortex Hormones/therapeutic use
Biopsy
Humans
Kidney Function Tests
Male
Middle Aged
Renal Dialysis
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Nm] Name of substance:0 (Adrenal Cortex Hormones); 0 (Anti-Infective Agents, Local); 85H0HZU99M (Povidone-Iodine)
[Em] Entry month:1801
[Cu] Class update date: 180115
[Lr] Last revision date:180115
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180110
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008879

  5 / 1757 MEDLINE  
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[PMID]: 29268755
[Au] Autor:Dumková J; Smutná T; Vrlíková L; Le Coustumer P; Vecera Z; Docekal B; Mikuska P; Capka L; Fictum P; Hampl A; Buchtová M
[Ad] Address:Department of Histology and Embryology, Faculty of Medicine, Masaryk University, 625 00, Brno, Czech Republic.
[Ti] Title:Sub-chronic inhalation of lead oxide nanoparticles revealed their broad distribution and tissue-specific subcellular localization in target organs.
[So] Source:Part Fibre Toxicol;14(1):55, 2017 12 21.
[Is] ISSN:1743-8977
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Lead is well known environmental pollutant, which can cause toxic effects in multiple organ systems. However, the influence of lead oxide nanoparticles, frequently emitted to the environment by high temperature technological processes, is still concealed. Therefore, we investigate lead oxide nanoparticle distribution through the body upon their entry into lungs and determine the microscopic and ultramicroscopic changes caused by the nanoparticles in primary and secondary target organs. METHODS: Adult female mice (ICR strain) were continuously exposed to lead oxide nanoparticles (PbO-NPs) with an average concentration approximately 10 particles/cm for 6 weeks (24 h/day, 7 days/week). At the end of the exposure period, lung, brain, liver, kidney, spleen, and blood were collected for chemical, histological, immunohistochemical and electron microscopic analyses. RESULTS: Lead content was found to be the highest in the kidney and lungs, followed by the liver and spleen; the smallest content of lead was found in brain. Nanoparticles were located in all analysed tissues and their highest number was found in the lung and liver. Kidney, spleen and brain contained lower number of nanoparticles, being about the same in all three organs. Lungs of animals exposed to lead oxide nanoparticles exhibited hyperaemia, small areas of atelectasis, alveolar emphysema, focal acute catarrhal bronchiolitis and also haemostasis with presence of siderophages in some animals. Nanoparticles were located in phagosomes or formed clusters within cytoplasmic vesicles. In the liver, lead oxide nanoparticle exposure caused hepatic remodeling with enlargement and hydropic degeneration of hepatocytes, centrilobular hypertrophy of hepatocytes with karyomegaly, areas of hepatic necrosis, occasional periportal inflammation, and extensive accumulation of lipid droplets. Nanoparticles were accumulated within mitochondria and peroxisomes forming aggregates enveloped by an electron-dense mitochondrial matrix. Only in some kidney samples, we observed areas of inflammatory infiltrates around renal corpuscles, tubules or vessels in the cortex. Lead oxide nanoparticles were dispersed in the cytoplasm, but not within cell organelles. There were no significant morphological changes in the spleen as a secondary target organ. Thus, pathological changes correlated with the amount of nanoparticles found in cells rather than with the concentration of lead in a given organ. CONCLUSIONS: Sub-chronic exposure to lead oxide nanoparticles has profound negative effects at both cellular and tissue levels. Notably, the fate and arrangement of lead oxide nanoparticles were dependent on the type of organs.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1712
[Cu] Class update date: 180108
[Lr] Last revision date:180108
[St] Status:In-Process
[do] DOI:10.1186/s12989-017-0236-y

  6 / 1757 MEDLINE  
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[PMID]: 28958692
[Au] Autor:Granado M; Amor S; Fernández N; Carreño-Tarragona G; Iglesias-Cruz MC; Martín-Carro B; Monge L; García-Villalón AL
[Ad] Address:Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma de Madrid, Madrid, Spain; CIBER Fisiopatologia de la Obesidad y Nutrición, Instituto de Salud Carlos III, Madrid, Spain. Electronic address: miriam.granado@uam.es.
[Ti] Title:Effects of early overnutrition on the renal response to Ang II and expression of RAAS components in rat renal tissue.
[So] Source:Nutr Metab Cardiovasc Dis;27(10):930-937, 2017 Oct.
[Is] ISSN:1590-3729
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND AND AIMS: The aim of this study was to analyze the effects of early overnutrition (EON) on the expression of the renin angiotensin aldosterone system (RAAS) components in renal cortex, renal arteries and renal perivascular adipose tissue (PVAT), as well as the vascular response of renal arteries to Angiotensin II (Ang II). METHODS AND RESULTS: On birth day litters were adjusted to twelve (L12-control) or three (L3-overfed) pups per mother. Half of the animals were sacrificed at weaning (21 days old) and the other half at 5 months of age. Ang II-induced vasoconstriction of renal artery segments increased in young overfed rats and decreased in adult overfed rats. EON decreased the gene expression of angiotensinogen (Agt), Ang II receptors AT1 and AT2 and eNOS in renal arteries of young rats, while it increased the mRNA levels of AT-2 and ET-1 in adult rats. In renal PVAT EON up-regulated the gene expression of COX-2 and TNF-α in young rats and the mRNA levels of renin receptor both in young and in adult rats. On the contrary, Ang II receptors mRNA levels were downregulated at both ages. Renal cortex of overfed rats showed increased gene expression of Agt in adult rats and of AT1 in young rats. However the mRNA levels of AT1 were decreased in the renal cortex of overfed adult rats. CONCLUSION: EON is associated with alterations in the vascular response of renal arteries to Ang II and changes in the gene expression of RAAS components in renal tissue.
[Mh] MeSH terms primary: Angiotensin II/pharmacology
Kidney/blood supply
Overnutrition/metabolism
Renal Artery/drug effects
Renin-Angiotensin System/drug effects
Vasoconstriction/drug effects
Vasoconstrictor Agents/pharmacology
[Mh] MeSH terms secundary: Adipose Tissue/drug effects
Adipose Tissue/metabolism
Adipose Tissue/physiopathology
Age Factors
Animal Nutritional Physiological Phenomena
Animals
Cyclooxygenase 2/genetics
Cyclooxygenase 2/metabolism
Disease Models, Animal
Dose-Response Relationship, Drug
Gene Expression Regulation
Nitric Oxide Synthase Type III/genetics
Nitric Oxide Synthase Type III/metabolism
Nutritional Status
Overnutrition/genetics
Overnutrition/physiopathology
RNA, Messenger/genetics
RNA, Messenger/metabolism
Rats, Sprague-Dawley
Receptor, Angiotensin, Type 1/genetics
Receptor, Angiotensin, Type 1/metabolism
Receptor, Angiotensin, Type 2/genetics
Receptor, Angiotensin, Type 2/metabolism
Renal Artery/metabolism
Renal Artery/physiopathology
Tumor Necrosis Factor-alpha/genetics
Tumor Necrosis Factor-alpha/metabolism
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (RNA, Messenger); 0 (Receptor, Angiotensin, Type 1); 0 (Receptor, Angiotensin, Type 2); 0 (Tumor Necrosis Factor-alpha); 0 (Vasoconstrictor Agents); 11128-99-7 (Angiotensin II); EC 1.14.13.39 (Nitric Oxide Synthase Type III); EC 1.14.13.39 (Nos3 protein, rat); EC 1.14.99.1 (Cyclooxygenase 2); EC 1.14.99.1 (Ptgs2 protein, rat)
[Em] Entry month:1710
[Cu] Class update date: 171030
[Lr] Last revision date:171030
[Js] Journal subset:IM
[Da] Date of entry for processing:170930
[St] Status:MEDLINE

  7 / 1757 MEDLINE  
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[PMID]: 28793394
[Au] Autor:Ko DH; Kim TH; Kim JW; Gu JJ; Yoon BH; Oh JH; Hong SG
[Ad] Address:Department of Internal Medicine, SAM Anyang Hospital, Anyang, Korea.
[Ti] Title:Tranexamic Acid-Induced Acute Renal Cortical Necrosis in Post-Endoscopic Papillectomy Bleeding.
[So] Source:Clin Endosc;, 2017 Aug 09.
[Is] ISSN:2234-2400
[Cp] Country of publication:Korea (South)
[La] Language:eng
[Ab] Abstract:Acute renal failure can be the result of acute renal cortical necrosis (RCN), which commonly occurs from complications occurring during pregnancy. RCN is rarely caused by medications, although tranexamic acid, which is used in patients with acute bleeding for its antifibrinolytic effects, reportedly causes acute RCN in rare cases. An 82-year-old woman experienced gastrointestinal bleeding after endoscopic papillectomy of an ampullary adenoma. The bleeding was controlled with tranexamic acid administration; however, 4 days later, her urine volume decreased and she developed pulmonary edema and dyspnea. Serum creatinine levels increased from 0.8 to 3.9 mg/dL and dialysis was performed. Abdominal pelvic computed tomography with contrast enhancement revealed bilateral RCN with no renal cortex enhancement. Renal dysfunction and oliguria persisted and hemodialysis was continued. Clinicians must be aware that acute RCN can occur after tranexamic acid administration to control bleeding.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1708
[Cu] Class update date: 170809
[Lr] Last revision date:170809
[St] Status:Publisher
[do] DOI:10.5946/ce.2017.021

  8 / 1757 MEDLINE  
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[PMID]: 28782620
[Au] Autor:Koh W; Shin JS; Lee J; Lee IH; Lee SK; Ha IH; Chung HJ
[Ad] Address:Jaseng Spine and Joint Research Institute, Jaseng Medical Foundation, Seoul, Republic of Korea. Electronic address: wkoh1231@gmail.com.
[Ti] Title:Anti-inflammatory effect of Cortex Eucommiae via modulation of the toll-like receptor 4 pathway in lipopolysaccharide-stimulated RAW 264.7 macrophages.
[So] Source:J Ethnopharmacol;209:255-263, 2017 Sep 14.
[Is] ISSN:1872-7573
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:ETHNOPHARMOCOLOGICAL RELEVANCE: Cortex Eucommiae (CE), the bark of Eucommia ulmoides Oliv., has been traditionally used for its kidney-tonifying and bone- and tendon-enhancing properties in Korea, China, and Japan. CE has been historically prescribed for inflammatory conditions such as arthritis of the knee and ankle. AIM OF THE STUDY: Although CE has recently been shown to suppress inflammation in scientific studies, whether this effect involves modulation of the toll-like receptor 4 (TLR-4) pathway is currently unknown. MATERIALS AND METHODS: The modulatory effect of CE on the TLR-4 pathway, both myeloid differentiation primary response gene 88 (Myd88)-dependent and independent, was investigated through real-time reverse transcriptase-polymerase chain reaction (RT-PCR), western blotting, and a reporter gene assay in lipopolysaccharide (LPS)-stimulated RAW 264.7 murine macrophages. RESULTS: CE dose-dependently inhibited nitric oxide production without significant cytotoxicity with an IC of 356.23µg/mL. In addition, CE down-regulated both LPS-induced mRNA and protein expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α), and interleukin-1ß (IL-1ß) in a dose-dependent manner. CE suppressed LPS-induced activation of nuclear factor-κB (NF-κB) and the mitogen-activated protein kinase (MAPK) pathways, which together comprise the Myd88-dependent TLR-4 pathway. The phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway was also down-regulated by CE in a dose-dependent manner. CE additionally suppressed LPS-induced activation of interferon-ß (IFN-ß) and signal transducer and activator of transcription (STAT) pathway, which is associated with the Myd88-independent TLR-4 pathway. CONCLUSIONS: CE down-regulated both Myd88-dependent and independent TLR-4 pathways, thus exerting anti-inflammatory effects. These results suggest that CE may be used as a potential therapeutic agent against chronic inflammatory diseases.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1708
[Cu] Class update date: 170828
[Lr] Last revision date:170828
[St] Status:In-Process

  9 / 1757 MEDLINE  
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[PMID]: 28774741
[Au] Autor:Tsamouri MM; Rapti M; Kouka P; Nepka C; Tsarouhas K; Soumelidis A; Koukoulis G; Tsatsakis A; Kouretas D; Tsitsimpikou C
[Ad] Address:Department of Biochemistry-Biotechnology, School of Health Sciences, University of Thessaly, Viopolis, Larissa, 41500, Greece.
[Ti] Title:Histopathological evaluation and redox assessment in blood and kidney tissues in a rabbit contrast-induced nephrotoxicity model.
[So] Source:Food Chem Toxicol;108(Pt A):186-193, 2017 Oct.
[Is] ISSN:1873-6351
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Contrast-induced nephropathy (CIN) is a leading cause of hospital-acquired acute kidney injury as a result of iodinated contrast-media use for diagnostic purposes. Pathophysiology remains unclear. In the present study iopromide was administered to New Zealand white rabbits without any prior intervention. Oxidative stress was assessed in blood and tissue level at three anatomical kidney areas (medullary, cortical, juxtamedullary). Histopathological evaluation was also performed. Serum creatinine and urea increased in the CIN groups over 25% at two hours after administration and returned to baseline at 48 h. In kidney tissues, a significant reduction (40%) of catalase in renal cortexes of the CIN groups was observed. Necrosis and tubular vacuolization was also noted that correlated with urea and creatinine levels. Lipid peroxidation decreased at 10 h after administration (>45%) and remained low even at 48 h. Plasma protein carbonyls were significantly increased (67%) in 2 h and dropped later. Serum levels of creatinine and urea at 24 and 48 h significantly correlated with the Total Antioxidant Activity and lipid peroxidation, respectively. Oxidative stress is shown to be involved in CIN development in the rabbit, with more pronounced effects to be confined to the cortex and outer stripe of the outer medulla.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1708
[Cu] Class update date: 170904
[Lr] Last revision date:170904
[St] Status:In-Process

  10 / 1757 MEDLINE  
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[PMID]: 28701229
[Au] Autor:Zhang BF; Wang PF; Cong YX; Lei JL; Wang H; Huang H; Han S; Zhuang Y
[Ad] Address:Department of Orthopedic trauma, Honghui Hospital, College of Medicine, Xi'an Jiaotong University, Beilin District, No. 555 Youyi East Road, 710054, Xi'an, Shaanxi Province, People's Republic of China.
[Ti] Title:Anti-high mobility group box-1 (HMGB1) antibody attenuates kidney damage following experimental crush injury and the possible role of the tumor necrosis factor-α and c-Jun N-terminal kinase pathway.
[So] Source:J Orthop Surg Res;12(1):110, 2017 Jul 12.
[Is] ISSN:1749-799X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Inflammation plays a crucial role in kidney damage after crush syndrome (CS). Several researchers report that high mobility group box-1 protein (HMGB1) may be the vital trigger in kidney damage, and tumor necrosis factor-α (TNF-α) and c-Jun N-terminal kinase (JNK) are involve in this pathophysiological process, but their biological roles are unclear. This study aimed to explore the relationship between HMGB1, JNK, and TNF-α in kidney damage. METHODS: The crush injury model was established using weight compression. The reliability of the crush injury model was determined by hematoxylin-eosin (HE) staining. Western blot was used to detect the expression of HMGB1, JNK, and TNF-α, and TUNEL was used to mark apoptotic cells in the renal cortex. RESULTS: The results showed that the highest expression of HMGB1 in muscle was 12 h after CS. JNK and TNF-α increased and peaked at 1 day after CS in kidneys. Western blot analysis revealed that anti-HMGB1 antibody could downregulate the expression of JNK and TNF-α. Anti-TNF-α could downregulate activation of JNK, and SP600125 could downregulate expression of TNF-α in the kidneys. In addition, anti-HMGB1 antibody, anti-TNF-α antibody, and SP600125 could reduce cellular apoptosis in the renal cortex. CONCLUSIONS: It is possible that JNK and TNF-α commonly contribute to kidney damage by assembling a positive feedback cycle after CS, leading to increased apoptosis in the renal cortex. HMGB1 from the muscle may be the trigger.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1707
[Cu] Class update date: 170718
[Lr] Last revision date:170718
[St] Status:In-Process
[do] DOI:10.1186/s13018-017-0614-z


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