Database : MEDLINE
Search on : Peritoneal and Fibrosis [Words]
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[PMID]: 29507108
[Au] Autor:Sun C; Chen SY
[Ad] Address:Department of Physiology and Pharmacology, University of Georgia, Athens, GA 30602.
[Ti] Title:RGC32 Promotes Bleomycin-Induced Systemic Sclerosis in a Murine Disease Model by Modulating Classically Activated Macrophage Function.
[So] Source:J Immunol;, 2018 Mar 05.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Systemic sclerosis (SSc) is a multisystem autoimmune disorder that is characterized by inflammation and fibrosis in the skin and internal organs. Previous studies indicate that inflammatory cells and cytokines play essential roles in the pathogenesis of SSc; however, the mechanisms that underlie the inflammation-driven development of SSc are not fully understood. In this study, we show that response gene to complement 32 (RGC32) is abundantly expressed in mouse macrophages in the early stage of bleomycin-induced SSc. Importantly, RGC32 is required to induce the inflammatory response during the onset of SSc, because RGC32 deficiency in mice significantly ameliorates skin and lung sclerosis and inhibits the expression of inflammatory mediators inducible NO synthase (iNOS) and IL-1ß in macrophages. RGC32 appears to be a novel regulator for the differentiation of classically activated macrophages (M1 macrophages). IFN-γ and LPS stimulation induces RGC32 expression in primary peritoneal macrophages and bone marrow-derived macrophages. RGC32 deficiency impairs the polarization of M1 macrophages and attenuates iNOS and IL-1ß production. Mechanistically, RGC32 interacts with NF-κB proteins and promotes iNOS and IL-1ß expression by binding to their promoters. Collectively, our data reveal that RGC32 promotes the onset of SSc by regulating the inflammatory response of M1 macrophages, and it may serve as a promising therapeutic target for treating SSc.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher

  2 / 3525 MEDLINE  
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[PMID]: 29521830
[Au] Autor:Kuckelman JP; Kononchik J; Smith J; Kniery KR; Kay JT; Hoffer ZS; Steele SR; Sohn V
[Ad] Address:Department of General Surgery, Madigan Army Medical Center, Tacoma, Washington.
[Ti] Title:Human-Derived Amniotic Membrane Is Associated With Decreased Postoperative Intraperitoneal Adhesions in a Rat Model.
[So] Source:Dis Colon Rectum;61(4):484-490, 2018 Apr.
[Is] ISSN:1530-0358
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Complications from adhesions after intra-abdominal surgery accounts for ~6% of hospital admissions. Currently, hyaluronate/carboxymethylcellulose represents the main option to prevent postoperative adhesion formation. Human amniotic membrane contains inherent anti-inflammatory properties that mitigate adhesion formation. OBJECTIVE: This study aimed to evaluate adhesion generation after surgical trauma with amniotic membranes compared with standard intraperitoneal adhesion barriers. DESIGN: This study is a double-blinded, prospective evaluation. SETTING: This study was conducted at an animal research facility. ANIMALS: Forty male rats were studied. INTERVENTION: Laparotomy was performed with peritoneal disruption to the cecum. Animals were randomly assigned to 1 of 5 groups: sham, control, saline, hyaluronic acid membrane, or amniotic membrane. Animals were euthanized at 14 days. MAIN OUTCOME MEASURES: Independent gross and histological assessments of adhesions were analyzed between groups by using adhesion scoring and microscopy. Scoring was based on the percentage of the cecum involved (0-4), vascularity of adhesions (0-3), strength (0-3), inflammation (0-3), and fibrosis (0-3). Adhered tissue was harvested for polymerase chain reaction analysis for gene regulation activity. RESULTS: All rats survived 14 days. Adhesions were observed in all animals. There were significantly fewer adhesions in the amniotic membrane group (2) versus hyaluronic acid (3) group (p = 0.01). The percentage of adhesion to the cecum was lower in the amniotic membrane group (29%) than in the hyaluronic acid group (47%, p = 0.04). Histological examination showed no significant difference between or within the 3 groups for inflammation or fibrosis. Genetic analysis of adhered tissues supported high rates of epithelialization and inhibition of fibrosis in the amniotic membrane group. LIMITATIONS: We are limited by the small sample size and the preclinical nature of the study. CONCLUSION: Human-derived amniotic membrane is effective at reducing intraperitoneal adhesion after surgical trauma and is superior to the current antiadhesion barriers. Amniotic membranes are well absorbed and demonstrate short-term safety. See Video Abstract at http://links.lww.com/DCR/A554.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1097/DCR.0000000000001037

  3 / 3525 MEDLINE  
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[PMID]: 29513881
[Au] Autor:Lopes LB; Abreu CC; Souza CF; Guimaraes LER; Silva AA; Aguiar-Alves F; Kidd KO; Kmoch S; Bleyer AJ; Almeida JR
[Ad] Address:Laboratório Multiusuário de Apoio è Pesquisa em Nefrologia e Ciências Médicas (LAMAP), Departamento de Patologia, Faculdade de Medicina, Universidade Federal Fluminense, Niterói, RJ, Brasil.
[Ti] Title:Identification of a novel UMOD mutation (c.163G>A) in a Brazilian family with autosomal dominant tubulointerstitial kidney disease.
[So] Source:Braz J Med Biol Res;51(3):e6560, 2018 Mar 01.
[Is] ISSN:1414-431X
[Cp] Country of publication:Brazil
[La] Language:eng
[Ab] Abstract:Autosomal dominant tubulointerstitial kidney disease (ADTKD) is characterized by autosomal dominant inheritance, progressive chronic kidney disease, and a bland urinary sediment. ADTKD is most commonly caused by mutations in the UMOD gene encoding uromodulin (ADTKD-UMOD). We herein report the first confirmed case of a multi-generational Brazilian family with ADTKD-UMOD, caused by a novel heterozygous mutation (c.163G>A, GGC→AGC, p.Gly55Ser) in the UMOD gene. Of 41 family members, 22 underwent genetic analysis, with 11 individuals found to have this mutation. Three affected individuals underwent hemodialysis, one peritoneal dialysis, and one patient received a kidney transplant from a family member later found to be genetically affected. Several younger individuals affected with the mutation were also identified. Clinical characteristics included a bland urinary sediment in all tested individuals and a kidney biopsy in one individual showing tubulointerstitial fibrosis. Unlike most other reported families with ADTKD-UMOD, neither gout nor hyperuricemia was found in affected individuals. In summary, we report a novel UMOD mutation in a Brazilian family with 11 affected members, and we discuss the importance of performing genetic testing in families with inherited kidney disease of unknown cause.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Process

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[PMID]: 29513812
[Au] Autor:Goret CC; Goret NE; Kiraz A; Ozkan OF; Karaayvaz M
[Ad] Address:Assistant Professor, Department of Surgical Pathology, Health Sciences University, Sancaktepe Research and Education Hospital, Istanbul, Turkey. Scientific, intellectual, conception and design of the study; analysis and interpretation of data; histopathological examinations; technical procedures; st
[Ti] Title:The effect of pycnogenol on lymphatic nodes and adhesion during in a peritoneal adhesion model in rats.
[So] Source:Acta Cir Bras;33(2):134-143, 2018 Feb.
[Is] ISSN:1678-2674
[Cp] Country of publication:Brazil
[La] Language:eng
[Ab] Abstract:PURPOSE: To investigate the effects of pycnogenol on peritoneal adhesions and additionally to investigate the immunohistochemical effects of free oxygen radicals and reactive lymph nodes detected in the adhesive tissue that was sampled surrounding the cecum on intra-abdominal adhesions. METHODS: Twenty-seven Wistar Albino rats were divided into three groups. In group 1 (sham), laparotomy was performed and stitched up. In group 2 (control), after laparotomy was performed, punctate hemorrhage was induced by cecal abrasion in the cecum and each rat was intraperitoneally administered 2 cc of saline. In group 3 (experimental), after laparotomy was performed, punctate hemorrhage was induced by cecal abrasion in the cecum and each rat was intraperitoneally administered a sterile Pycnogenol derivative. The rats in all groups were re-laparotomized on postoperative day 7; samples were obtained from the peritoneal tissue surrounding the cecum, and the rats were sacrificed. RESULTS: In group 3, there was a statistically significant difference in terms of inflammation, lymph node size, and free oxygen radicals; these parameters tended to increase. In terms of fibrosis evaluated using H&E and MT, there was no significant difference between groups 2 and 3. CONCLUSIONS: No positive outcomes indicating that pycnogenol reduces intra-abdominal adhesions were obtained. However, it caused severe inflammation in the tissue. Moreover, a significant increase in lymph node size was detected secondary to inflammation. Additionally, in immunohistochemical analyses conducted to detect oxidative stress, pycnogenol increased the production of free oxygen radicals in the tissue.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Process

  5 / 3525 MEDLINE  
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[PMID]: 29208752
[Au] Autor:Herzog R; Boehm M; Unterwurzacher M; Wagner A; Parapatics K; Májek P; Mueller AC; Lichtenauer A; Bennett KL; Alper SL; Vychytil A; Aufricht C; Kratochwill K
[Ad] Address:From the ‡Division of Pediatric Nephrology and Gastroenterology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Vienna, Austria.
[Ti] Title:Effects of Alanyl-Glutamine Treatment on the Peritoneal Dialysis Effluent Proteome Reveal Pathomechanism-Associated Molecular Signatures.
[So] Source:Mol Cell Proteomics;17(3):516-532, 2018 Mar.
[Is] ISSN:1535-9484
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Peritoneal dialysis (PD) is a modality of renal replacement therapy in which the high volumes of available PD effluent (PDE) represents a rich source of biomarkers for monitoring disease and therapy. Although this information could help guide the management of PD patients, little is known about the potential of PDE to define pathomechanism-associated molecular signatures in PD.We therefore subjected PDE to a high-performance multiplex proteomic analysis after depletion of highly-abundant plasma proteins and enrichment of low-abundance proteins. A combination of label-free and isobaric labeling strategies was applied to PDE samples from PD patients ( = 20) treated in an open-label, randomized, two-period, cross-over clinical trial with standard PD fluid or with a novel PD fluid supplemented with alanyl-glutamine (AlaGln).With this workflow we identified 2506 unique proteins in the PDE proteome, greatly increasing coverage beyond the 171 previously-reported proteins. The proteins identified range from high abundance plasma proteins to low abundance cellular proteins, and are linked to larger numbers of biological processes and pathways, some of which are novel for PDE. Interestingly, proteins linked to membrane remodeling and fibrosis are overrepresented in PDE compared with plasma, whereas the proteins underrepresented in PDE suggest decreases in host defense, immune-competence and response to stress. Treatment with AlaGln-supplemented PD fluid is associated with reduced activity of membrane injury-associated mechanisms and with restoration of biological processes involved in stress responses and host defense.Our study represents the first application of the PDE proteome in a randomized controlled prospective clinical trial of PD. This novel proteomic workflow allowed detection of low abundance biomarkers to define pathomechanism-associated molecular signatures in PD and their alterations by a novel therapeutic intervention.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Data-Review
[do] DOI:10.1074/mcp.RA117.000186

  6 / 3525 MEDLINE  
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[PMID]: 29390323
[Au] Autor:Xiang D; He J; Wang H; Xiong F; Cheng H; Ai J; Shan R; Wan R; Zhang L; Shi J
[Ad] Address:Department of General Surgery, The First Affiliated Hospital of Nanchang University.
[Ti] Title:Liver transplantation for decompensated liver cirrhosis caused by progressive familial intrahepatic cholestasis type 3: A case report.
[So] Source:Medicine (Baltimore);96(50):e9158, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:RATIONALE: Progressive familial intrahepatic cholestasis (PFIC) type 3, characterized by high gamma glutamyl transferase (GGT), is an autosomal recessive genetic disease. It often occurs in patients' first years of age. However, high GGT type PFIC is still rare. PATIENT CONCERNS: The present study reports a case of liver transplantation for decompensated liver cirrhosis caused by PFIC type 3. An 18-year-old male presented with a history of abdominal distension and jaundice for 2 months. He had abdominal tenderness but no rebounding pain. Moreover, his dullness was felt over the liver and the spleen was palpable 8 cm below the ribs. DIAGNOSES: Computed tomography and magnetic resonance cholangiopancreato graphy of the upper abdomen revealed cirrhosis, portal hypertension, collateral circulation formation, large spleen, and ascites. Blood biochemistry showed high alanine transaminase, aspartate transaminase, and GGT. The diagnosis of decompensated liver cirrhosis caused by PFIC-3 was finally confirmed by plasma gene detecting. INTERVENTIONS: The patient received an open surgery named allogeneic liver transplantation after successful matching of immune types between the recipient and donor. Peritoneal puncture and catheter drainage under B-ultrasound was performed when an encapsulated effusion between the liver and stomach arose. OUTCOMES: The patient was discharged without specific discomfort and was almost free of fluid accumulation 51 days after the surgery. At the 6-month follow-up, he had no discomfort and the blood routine, liver functions showed no abnormalities. LESSONS: We found a new mutant fragment of ABCB4 gene in the process of diagnosis. Liver transplantation remains the most definitive treatment for PFIC. Current medical therapies and surgical interventions such as biliary diversion have potentially created a synergistic outcome.
[Mh] MeSH terms primary: ATP Binding Cassette Transporter, Sub-Family B/deficiency
Cholestasis, Intrahepatic/complications
Liver Cirrhosis/etiology
Liver Cirrhosis/surgery
Liver Transplantation
[Mh] MeSH terms secundary: Adolescent
Humans
Liver Cirrhosis/diagnostic imaging
Male
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Nm] Name of substance:0 (ATP Binding Cassette Transporter, Sub-Family B)
[Em] Entry month:1802
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009158

  7 / 3525 MEDLINE  
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[PMID]: 29467297
[Au] Autor:Takemura N; Kurashima Y; Mori Y; Okada K; Ogino T; Osawa H; Matsuno H; Aayam L; Kaneto S; Park EJ; Sato S; Matsunaga K; Tamura Y; Ouchi Y; Kumagai Y; Kobayashi D; Suzuki Y; Yoshioka Y; Nishimura J; Mori M; Ishii KJ; Rothenberg ME; Kiyono H; Akira S; Uematsu S
[Ad] Address:Department of Mucosal Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.
[Ti] Title:Eosinophil depletion suppresses radiation-induced small intestinal fibrosis.
[So] Source:Sci Transl Med;10(429), 2018 Feb 21.
[Is] ISSN:1946-6242
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Radiation-induced intestinal fibrosis (RIF) is a serious complication after abdominal radiotherapy for pelvic tumor or peritoneal metastasis. Herein, we show that RIF is mediated by eosinophil interactions with α-smooth muscle actin-positive (α-SMA ) stromal cells. Abdominal irradiation caused RIF especially in the submucosa (SM) of the small intestine, which was associated with the excessive accumulation of eosinophils in both human and mouse. Eosinophil-deficient mice showed markedly ameliorated RIF, suggesting the importance of eosinophils. After abdominal irradiation, chronic crypt cell death caused elevation of extracellular adenosine triphosphate, which in turn activated expression of C-C motif chemokine 11 (CCL11) by pericryptal α-SMA cells in the SM to attract eosinophils in mice. Inhibition of C-C chemokine receptor 3 (CCR3) by genetic deficiency or neutralizing antibody (Ab) treatment suppressed eosinophil accumulation in the SM after irradiation in mice, suggesting a critical role of the CCL11/CCR3 axis in the eosinophil recruitment. Activated α-SMA cells also expressed granulocyte-macrophage colony-stimulating factor (GM-CSF) to activate eosinophils. Transforming growth factor-ß1 from GM-CSF-stimulated eosinophils promoted collagen expression by α-SMA cells. In translational studies, treatment with a newly developed interleukin-5 receptor α-targeting Ab, analogous to the human agent benralizumab, depleted intestinal eosinophils and suppressed RIF in mice. Collectively, we identified eosinophils as a crucial factor in the pathogenesis of RIF and showed potential therapeutic strategies for RIF by targeting eosinophils.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180222
[Lr] Last revision date:180222
[St] Status:In-Data-Review

  8 / 3525 MEDLINE  
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[PMID]: 29422602
[Au] Autor:Oba-Yabana I; Mori T; Takahashi C; Hirose T; Ohsaki Y; Kinugasa S; Muroya Y; Sato E; Nguyen G; Piedagnel R; Ronco PM; Totsune K; Ito S
[Ad] Address:Division of Nephrology, Endocrinology and Vascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.
[Ti] Title:Acidic organelles mediate TGF-ß1-induced cellular fibrosis via (pro)renin receptor and vacuolar ATPase trafficking in human peritoneal mesothelial cells.
[So] Source:Sci Rep;8(1):2648, 2018 Feb 08.
[Is] ISSN:2045-2322
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:TGF-ß1, which can cause renal tubular injury through a vacuolar-type H -ATPase (V-ATPase)-mediated pathway, is induced by the glucose degradation product methylglyoxal to yield peritoneal injury and fibrosis. The present study investigated the roles of V-ATPase and its accessory protein, the (pro)renin receptor, in peritoneal fibrosis during peritoneal dialysis. Rats daily administered 20 mM methylglyoxal intraperitoneally developed significant peritoneal fibrosis after 7 days with increased expression of TGF-ß and V-ATPase, which was reduced by the inhibition of V-ATPase with co-administration of 100 mM bafilomycin A1. The (pro)renin receptor and V-ATPase were expressed in acidic organelles and cell membranes of human peritoneal mesothelial cells. TGF-ß1 upregulated the expression of collagens, α-SMA, and EDA-fibronectin, together with ERK1/2 phosphorylation, which was reduced by inhibition of V-ATPase, (pro)renin receptor, or the MAPK pathway. Fibronectin and the soluble (pro)renin receptor were excreted from cells by acidic organelle trafficking in response to TGF-ß1; this excretion was also suppressed by inhibition of V-ATPase. Soluble (pro)renin receptor concentrations in effluents of patients undergoing peritoneal dialysis were associated with the dialysate-to-plasma ratio of creatinine. Together, these results demonstrate a novel fibrosis mechanism through the (pro)renin receptor and V-ATPase in the acidic organelles of peritoneal mesothelial cells.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180218
[Lr] Last revision date:180218
[St] Status:In-Data-Review
[do] DOI:10.1038/s41598-018-20940-x

  9 / 3525 MEDLINE  
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[PMID]: 29450853
[Au] Autor:Foti PV; Farina R; Palmucci S; Vizzini IAA; Libertini N; Coronella M; Spadola S; Caltabiano R; Iraci M; Basile A; Milone P; Cianci A; Ettorre GC
[Ad] Address:Radiodiagnostic and Radiotherapy Unit, University Hospital "Policlinico-Vittorio Emanuele", Via Santa Sofia 78, 95123, Catania, Italy. pietrofoti@hotmail.com.
[Ti] Title:Endometriosis: clinical features, MR imaging findings and pathologic correlation.
[So] Source:Insights Imaging;, 2018 Feb 15.
[Is] ISSN:1869-4101
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:OBJECTIVE: We illustrate the magnetic resonance imaging (MRI) features of endometriosis. BACKGROUND: Endometriosis is a chronic gynaecological condition affecting women of reproductive age and may cause pelvic pain and infertility. It is characterized by the growth of functional ectopic endometrial glands and stroma outside the uterus and includes three different manifestations: ovarian endometriomas, peritoneal implants, deep pelvic endometriosis. The primary locations are in the pelvis; extrapelvic endometriosis may rarely occur. Diagnosis requires a combination of clinical history, invasive and non-invasive techniques. The definitive diagnosis is based on laparoscopy with histological confirmation. Diagnostic imaging is necessary for treatment planning. MRI is as a second-line technique after ultrasound. The MRI appearance of endometriotic lesions is variable and depends on the quantity and age of haemorrhage, the amount of endometrial cells, stroma, smooth muscle proliferation and fibrosis. The purpose of surgery is to achieve complete resection of all endometriotic lesions in the same operation. CONCLUSION: Owing to the possibility to perform a complete assessment of all pelvic compartments at one time, MRI represents the best imaging technique for preoperative staging of endometriosis, in order to choose the more appropriate surgical approach and to plan a multidisciplinary team work. TEACHING POINTS: • Endometriosis includes ovarian endometriomas, peritoneal implants and deep pelvic endometriosis. • MRI is a second-line imaging technique after US. • Deep pelvic endometriosis is associated with chronic pelvic pain and infertility. • Endometriosis is characterized by considerable diagnostic delay. • MRI is the best imaging technique for preoperative staging of endometriosis.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1802
[Cu] Class update date: 180216
[Lr] Last revision date:180216
[St] Status:Publisher
[do] DOI:10.1007/s13244-017-0591-0

  10 / 3525 MEDLINE  
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[PMID]: 29444417
[Au] Autor:Shoeib HM; Keshk WA; Foda AM; Abo El Noeman SEAE
[Ad] Address:Tanta University Faculty of Medicine, 68782, medical biochemistry, Tanta, Egypt ; hshoiep@yahoo.com.
[Ti] Title:A study on the Regenerative Effect of Platelets Rich Plasma on Experimentally Induced Hepatic Damage In Albino Rats.
[So] Source:Can J Physiol Pharmacol;, 2018 Feb 14.
[Is] ISSN:1205-7541
[Cp] Country of publication:Canada
[La] Language:eng
[Ab] Abstract:Hepatic fibrosis is a worldwide health problem with significant morbidity and mortality. Currently, there is no effective therapy for hepatic fibrosis. So that the present study was aimed to evaluate the possible regenerative effect of Platelet-rich plasma (PRP) against thioacetamide (TAA) induced hepatic damage. Eighty albino rats were included; 40 were used for PRP preparation and 40 were randomly divided into four groups. Group I (control group); group II (PRP control); group III (TAA- intoxicated in a dose of 200 mg ∕ kg body weight/twice weekly for 7 weeks, intra-peritoneal and group IV (TAA-intoxicated+ PRP treated). Macrophage inflammatory protein-1α (MIP-1α) and cyclic adenosine monophosphate (cAMP) were immunoassayed in addition to peroxinitrite level, NADPH-quinine oxido-reductase-1 (NQO1) enzyme activity and liver function. PRP treatment showed significant improvement in hepatic function, decreased MIP-1α and peroxinitrite level. Meanwhile, significant increase in NQO1 enzyme activity and cAMP level were observed. The histopathological results confirmed the laboratory results with improvement of hepatic architecture except for some inflammatory cellular infiltrates. IN CONCLUSION: PRP has the ability to protect against TAA-induced liver damage possibly by improving redox status, liver histopathological architecture, disruption of the inflammatory and fibrotic response induced by TAA.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180214
[Lr] Last revision date:180214
[St] Status:Publisher
[do] DOI:10.1139/cjpp-2017-0738


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