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[PMID]: 29524844
[Au] Autor:Cheng Z; Shen X; Jiang X; Shan H; Cimini M; Fang P; Ji Y; Park JY; Drosatos K; Yang X; Kevil CG; Kishore R; Wang H
[Ad] Address:Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, 3500 Broad Street, Philadelphia, PA 19140, USA. Electronic address: zjcheng@temple.edu.
[Ti] Title:Hyperhomocysteinemia potentiates diabetes-impaired EDHF-induced vascular relaxation: Role of insufficient hydrogen sulfide.
[So] Source:Redox Biol;16:215-225, 2018 Feb 14.
[Is] ISSN:2213-2317
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Insufficient hydrogen sulfide (H S) has been implicated in Type 2 diabetic mellitus (T2DM) and hyperhomocysteinemia (HHcy)-related cardiovascular complications. We investigated the role of H S in T2DM and HHcy-induced endothelial dysfunction in small mesenteric artery (SMA) of db/db mice fed a high methionine (HM) diet. HM diet (8 weeks) induced HHcy in both T2DM db/db mice and non-diabetic db/+ mice (total plasma Hcy: 48.4 and 31.3 µM, respectively), and aggravated the impaired endothelium-derived hyperpolarization factor (EDHF)-induced endothelium-dependent relaxation to acetylcholine (ACh), determined by the presence of eNOS inhibitor N(ω)-nitro-L-arginine methyl ester (L-NAME) and prostacyclin (PGI ) inhibitor indomethacin (INDO), in SMA from db/db mice but not that from db/+ mice. A non-selective Ca -active potassium channel (K ) opener NS309 rescued T2DM/HHcy-impaired EDHF-mediated vascular relaxation to ACh. EDHF-induced relaxation to ACh was inhibited by a non-selective K blocker TEA and intermediate-conductance K blocker (IK ) Tram-34, but not by small-conductance K (SK ) blocker Apamin. HHcy potentiated the reduction of free sulfide, H S and cystathionine γ-lyase protein, which converts L-cysteine to H S, in SMA of db/db mice. Importantly, a stable H S donor DATS diminished the enhanced O production in SMAs and lung endothelial cells of T2DM/HHcy mice. Antioxidant PEG-SOD and DATS improved T2DM/HHcy impaired relaxation to ACh. Moreover, HHcy increased hyperglycemia-induced IK tyrosine nitration in human micro-vascular endothelial cells. EDHF-induced vascular relaxation to L-cysteine was not altered, whereas such relaxation to NaHS was potentiated by HHcy in SMA of db/db mice which was abolished by ATP-sensitive potassium channel blocker Glycolamide but not by K blockers. CONCLUSIONS: Intermediate HHcy potentiated H S reduction via CSE-downregulation in microvasculature of T2DM mice. H S is justified as an EDHF. Insufficient H S impaired EDHF-induced vascular relaxation via oxidative stress and IK inactivation in T2DM/HHcy mice. H S therapy may be beneficial for prevention and treatment of micro-vascular complications in patients with T2DM and HHcy.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 41220 MEDLINE  
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[PMID]: 29524409
[Au] Autor:Norris PC; Serhan CN
[Ad] Address:Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, 60 Fenwood Road, BTM 3016, Boston, MA, 02115, USA.
[Ti] Title:Metabololipidomic profiling of functional immunoresolvent clusters and eicosanoids in mammalian tissues.
[So] Source:Biochem Biophys Res Commun;, 2018 Mar 07.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Metabolomics enables a systems approach to interrogate the bioactive mediators, their pathways and further metabolites involved in the physiology and pathophysiology of human and animal tissues. New metabololipidomic approaches with mass spectrometry presented in this brief review can now be utilized for the identification and profiling of lipid mediator networks that control inflammation-resolution in human blood and healthy and diseased solid tissues. Coagulation of blood is a protective response that prevents excessive bleeding on injury of blood vessels. Here, we review novel approaches to understand the relationship(s) between coagulation and resolution of inflammation and infection. To determine whether coagulation is involved in host-protective actions by lipid mediators, we used a metabololipidomic-based profiling approach with human whole blood (WB) during coagulation. We identified recently temporal clusters of endogenously produced pro-thrombotic and proinflammatory lipid mediators (eicosanoids), as well as specialized proresolving mediators (SPMs) in this vital process. In addition to the classic eicosanoids (prostaglandins, thromboxanes and leukotrienes), a specific SPM cluster was identified that consists of resolvin E1 (RvE1), RvD1, RvD5, lipoxin B , and maresin 1, each of which present at bioactive concentrations (0.1-1 nM). The removal of adenosine from coagulating blood samples significantly enhances SPM amounts and unleashes the biosynthesis of RvD3, RvD4, and RvD6 evident following rapid snap freezing with centrifugation before extraction and LC-MS-MS. The classic cyclooxygenase inhibitors, celecoxib and indomethacin, that block thromboxanes and prostanoids do not block production of the clot-driven SPM cluster. Unbiased mass cytometry analysis demonstrated that the SPM cluster produced in human blood targets leukocytes at the single-cell level, directly activating extracellular signaling in human neutrophils and monocytes. Human whole blood treated with the components of this SPM cluster enhanced both phagocytosis and killing of Escherichia coli by leukocytes. Thus, we identified a pro-resolving lipid mediator circuit and specific SPM cluster that promotes host defense. This new lipid mediator (LM)-SPM metabololipidomic approach now provides accessible metabolomic profiles in healthy and diseased human tissues, including cancer, for precision and personalized medicine.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 41220 MEDLINE  
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[PMID]: 29501751
[Au] Autor:Zuliani JP; Gutiérrez JM; Teixeira C
[Ad] Address:Laboratório de Farmacologia, Instituto Butantan, Sao Paulo, Brazil; Laboratório de Imunologia Celular Aplicada à Saúde, Fundação Oswaldo Cruz Rondônia/FIOCRUZ-RO, Porto Velho, RO, Brazil; Dep. Medicina, Universidade Federal de Rondônia, UNIR, Porto Velho, RO, Brazil.
[Ti] Title:Signaling pathways involved in zymosan phagocytosis induced by two secreted phospholipases A isolated from Bothrops asper snake venom in macrophages.
[So] Source:Int J Biol Macromol;113:575-582, 2018 Mar 03.
[Is] ISSN:1879-0003
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Phagocytosis, a process involved in host defense, requires coordination of a variety of signaling reactions. MT-II, a catalytically-inactive Lys49-PLA ¸ and MT-III, an active Asp49-PLA isolated from Bothrops asper snake venom, activate phagocytosis in macrophages. In this study the signal pathways mediating zymosan phagocytosis, focusing in lipidic second messengers, were investigated. Macrophages collected from male Swiss mouse peritoneum were obtained 96h after i.p. injection of thioglycollate. Phagocytosis was evaluated with non-opsonized zymosan in the presence or absence of specific inhibitors. Data showed that both venom PLA s increased phagocytosis. Zileuton, Etoricoxib, PACOCF (5-LO, COX-2 and iPLA inhibitors, respectively), as well as WEB2170 (PAF receptor antagonist) significantly reduced phagocytosis induced by both venom PLA s. However, Indomethacin (COX-1/COX-2 inhibitor) and Montelukast (CysL receptor antagonist) did not affect the toxins-induced phagocytosis. Moreover, while PACOCF3 (iPLA inhibitor), reduced the phagocytosis induced by MT-II and MT-III, AACOCF (cPLA inhibitor) significantly reduced the MT-II, but not MT-III-induced phagocytosis. These data suggest the effect of both sPLA s depends on iPLA and that the effect of MT-II depends on activation of cPLA . COX-2 and 5-LO-derived metabolites as well as PAF are involved in the signaling events required for phagocytosis induced by both venom sPLA s.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  4 / 41220 MEDLINE  
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[PMID]: 29249749
[Au] Autor:Kaneda T; Kanda H; Tajima T; Urakawa N; Shimizu K
[Ad] Address:Laboratory of Veterinary Pharmacology, School of Veterinary Medicine, and Nippon Veterinary and Life Science University, 7-1 Kyonan-cho 1-chome, Musashino, Tokyo 180-8602, Japan.
[Ti] Title:Imidazole-induced contractions in bovine tracheal smooth muscle are not dependent on the cAMP pathway.
[So] Source:J Vet Med Sci;80(2):341-345, 2018 Mar 02.
[Is] ISSN:1347-7439
[Cp] Country of publication:Japan
[La] Language:eng
[Ab] Abstract:The mechanism of imidazole-induced contraction on the bovine tracheal smooth muscle was investigated. Imidazole induced muscle contraction in a concentration-dependent manner on bovine, porcine and guinea-pig tracheas, but not in rat or mouse. In bovine tracheas, imidazole was cumulatively applied and induced muscle tension and increasesd intracellular Ca level in a concentration -dependent manner. Imidazole, even at 300 µM, the concentration at which maximum contractile response occurs, did not significantly increase in cAMP content relative to control. Atropine inhibited imidazole-induced contraction at a concentration- dependent manner and pretreatment of hemicholinium-3 almost abolished imidazole-induced contraction. Conversely, pretreatment of tripelennamine, indomethacin or tetrodotoxin did not affect imidazole-induced contraction. Acetylcholine or eserine induced contraction in bovine, porcine, guinea pig, rat and mice trachea in a concentration-dependent manner. However, there was little difference in the rank order of maximum contraction of these agents. Imidazole-induced contraction was greater in bovine trachea compared to the other species tested. Further, cAMP did not appear to play a role in imidazole-induced contraction, suggesting other mechanisms, such as the release of endogenous acetylcholine.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.1292/jvms.17-0526

  5 / 41220 MEDLINE  
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[PMID]: 29523851
[Au] Autor:Shahin NN; Abdelkader NF; Safar MM
[Ad] Address:Department of Biochemistry, Faculty of Pharmacy, Cairo University, Cairo, Egypt.
[Ti] Title:A Novel Role of Irbesartan in Gastroprotection against Indomethacin-Induced Gastric Injury in Rats: Targeting DDAH/ADMA and EGFR/ERK Signaling.
[So] Source:Sci Rep;8(1):4280, 2018 Mar 09.
[Is] ISSN:2045-2322
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The advent of angiotensin II type 1 receptor blockers (ARBs) as intriguing gastroprotective candidates and the superior pharmacokinetics and pharmacodynamics displayed by irbesartan compared to many other ARBs raised the interest to investigate its gastroprotective potential in a rat model of gastric injury. Irbesartan (50 mg/Kg) was orally administered to male Wistar rats once daily for 14 days; thereafter gastric injury was induced by indomethacin (60 mg/Kg, p.o). Irbesartan reduced gastric ulcer index, gastric acidity, and ameliorated indomethacin-induced gastric mucosal apoptotic and inflammatory aberrations, as demonstrated by hampering caspase-3, prostaglandin E and tumor necrosis factor-alpha levels and cyclooxygenase-2 mRNA expression. This ARB increased mucosal dimethylarginine dimethylaminohydrolase-1 (DDAH-1) gene expression and decreased elevated levels of matrix metalloproteinase-9, asymmetric dimethylarginine (ADMA), epidermal growth factor receptor (EGFR) mRNA and phosphorylated extracellular signal-regulated kinase 1 and 2 (pERK1/2). Histopathological evaluation corroborated biochemical findings. Overall efficacy of irbesartan was comparable to ranitidine, the widely used H receptor blocker. In conclusion, irbesartan exerts significant gastroprotection against indomethacin-induced mucosal damage via acid-inhibitory, anti-inflammatory, anti-apoptotic and extracellular matrix remodeling mechanisms that are probably mediated, at least partly, by down-regulating DDAH/ADMA and EGFR/ERK1/2 signaling.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review
[do] DOI:10.1038/s41598-018-22727-6

  6 / 41220 MEDLINE  
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[PMID]: 29385210
[Au] Autor:Eadie LN; Dang P; Goyne JM; Hughes TP; White DL
[Ad] Address:Cancer Theme, South Australian Health and Medical Research Institute (SAHMRI), Adelaide, South Australia.
[Ti] Title:ABCC6 plays a significant role in the transport of nilotinib and dasatinib, and contributes to TKI resistance in vitro, in both cell lines and primary patient mononuclear cells.
[So] Source:PLoS One;13(1):e0192180, 2018.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:ATP Binding Cassette family efflux proteins ABCB1 and ABCG2 have previously been demonstrated to interact with Tyrosine Kinase Inhibitors (TKIs); however, evidence for the interaction of other potentially relevant drug transporters with TKIs is lacking. Through Taqman transporter array technology we assessed the impact of nilotinib on mRNA expression of ABC transporters, with ABCC6 identified as a transporter of interest. Additionally, increased expression of ABCC6 mRNA was observed during in vitro development of nilotinib resistance in BCR-ABL1-expressing cell lines. K562 cells exposed to gradually increasing concentrations of nilotinib (to 2 µM) expressed up to 57-fold higher levels of ABCC6 mRNA when compared with control cells (p = 0.002). Analogous results were observed in nilotinib resistant K562-Dox cells (up to 33-fold higher levels of ABCC6, p = 0.002). IC50 experiments were conducted on patient mononuclear cells in the absence and presence of three ABCC6 inhibitors: indomethacin, probenecid and pantoprazole. Results demonstrated that all three inhibitors significantly reduced nilotinib IC50 (p<0.001) indicating ABCC6 is likely involved in nilotinib transport. Cell line data confirmed these findings. Similar results were obtained for dasatinib, but not imatinib. Combined, these studies suggest that nilotinib and dasatinib are likely substrates of ABCC6 and to our knowledge, this is the first report of ABCC6 involvement in TKI transport. In addition, ABCC6 overexpression may also contribute to nilotinib and dasatinib resistance in vitro. With nilotinib and dasatinib now front line therapy options in the treatment of CML, concomitant administration of ABCC6 inhibitors may present an attractive option to enhance TKI efficacy.
[Mh] MeSH terms primary: Dasatinib/pharmacology
Leukocytes, Mononuclear/drug effects
Multidrug Resistance-Associated Proteins/physiology
Protein Kinase Inhibitors/pharmacology
Pyrimidines/pharmacology
[Mh] MeSH terms secundary: Cell Line
Dasatinib/pharmacokinetics
Drug Resistance, Neoplasm
Fusion Proteins, bcr-abl/metabolism
Humans
Multidrug Resistance-Associated Proteins/genetics
Protein Kinase Inhibitors/pharmacokinetics
Pyrimidines/pharmacokinetics
RNA, Messenger/genetics
Real-Time Polymerase Chain Reaction
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide); 0 (ABCC6 protein, human); 0 (Multidrug Resistance-Associated Proteins); 0 (Protein Kinase Inhibitors); 0 (Pyrimidines); 0 (RNA, Messenger); EC 2.7.10.2 (Fusion Proteins, bcr-abl); RBZ1571X5H (Dasatinib)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0192180

  7 / 41220 MEDLINE  
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[PMID]: 29484402
[Au] Autor:Hamam F; Eldalo A; Abdallah Q; Al-Deeb I; Alzahrani S; Alwagdani A; Alotaibi A; Nasr AR; Gouda Y; Mohamed K
[Ad] Address:Department of Pharmacology and Toxicology, College of Pharmacy, Taif University, Taif, Makkah 21974, Kingdom of Saudi Arabia.
[Ti] Title:Pharmacological activities of a novel plant species, Huernia Sp. Nov. aff. Boleana growing in the high mountains of southwest Saudi Arabia.
[So] Source:Mol Med Rep;17(4):6059-6067, 2018 Apr.
[Is] ISSN:1791-3004
[Cp] Country of publication:Greece
[La] Language:eng
[Ab] Abstract:Huernia Sp. Nov. aff. Boleana, Apocynaceae, grows in the high mountains of southwest Saudi Arabia and is widely used as a remedy for the treatment of diabetes. The present study investigated the anti­inflammatory, wound healing and inhibitory effects on migration of Huernia Sp. Nov. aff. Boleana. The anti­inflammatory effect was assessed in mice using formalin­induced edema. Wound healing effects were assessed in rats using a circular excision wound model. An in vitro 'scratch' test was used to investigate the inhibitory effects on melanoma cell (B16­F10) migration. The anti­inflammatory effects of total extract, hexane and chloroform fractions were greater or equal to indomethacin (control). The relatively non­polar fractions (hexane and chloroform) exhibited higher anti­inflammatory activities compared with the aqueous fraction. The percentage of wound contraction among animals treated with the plant extract was higher compared with the control; however, this difference was not statistically significant (P>0.05). The total plant extract increased wound healing by inhibiting the inflammatory response, promoting angiogenesis, and significantly promoting the proliferation of fibroblasts, particularly on days 7 and 14 post­wounding. Furthermore, the plant extract promoted wound repair via the enhancement of collagen synthesis, and complete epithelization with well­formed and differentiated epithelial tissues. The in vitro 'scratch' test indicated the inhibitory effects of this plant on melanoma cell migration in a dose­dependent manner. The present study indicated that Huernia Sp. Nov. aff. Boleana may have potential as an anti­inflammatory, wound-healing and migration-inhibiting ethno medicine.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process
[do] DOI:10.3892/mmr.2018.8607

  8 / 41220 MEDLINE  
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[PMID]: 29481945
[Au] Autor:Semjonov K; Salm M; Lipiäinen T; Kogermann K; Lust A; Laidmäe I; Antikainen O; Strachan CJ; Ehlers H; Yliruusi J; Heinämäki J
[Ad] Address:Institute of Pharmacy, Faculty of Medicine, University of Tartu, Nooruse Str. 1, EE-50411 Tartu, Estonia. Electronic address: kristian.semjonov@ut.ee.
[Ti] Title:Interdependence of particle properties and bulk powder behavior of indomethacin in quench-cooled molten two-phase solid dispersions.
[So] Source:Int J Pharm;541(1-2):188-197, 2018 Feb 24.
[Is] ISSN:1873-3476
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Solid dispersions (SDs) hold a proven potential in formulating poorly water-soluble drugs. The present paper investigates the interfacial phenomena associated with the bulk powder flow, water sorption, wetting and dissolution of the SDs prepared by a modified melt and quench-cooling (QC) method. Poorly water-soluble indomethacin (IND) was QC molten with solubilizing graft copolymer (Soluplus®) or polyol sugar alcohol (xylitol, XYL). The interfacial interactions of SDs with air/water were found to be reliant on the type (amorphous/crystalline) and amount of the carrier material used. The final SDs were composed of fused agglomerates (SOL) or large jagged particles (XYL) with good wetting and powder flow properties. The initial dissolution of IND was accelerated by both carrier materials studied. The QC molten SDs with amorphous Soluplus® significantly improved the dissolution rate of IND at pH 6.8 (79.9 ±â€¯0.2% at 30 min) compared to that of pure crystalline drug. The substantial improvement in the dissolution rate of IND was in connection with the amorphous state of the drug being stabilized by Soluplus® in the QC molten SDs. However, it is evident that a strong H-bond formation between the components in some regions of the QC molten SDs can limit the dissolution of IND. The QC molten two-phase SDs with a polyol carrier (XYL) showed rapid and continuous drug release without reaching a plateau.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher

  9 / 41220 MEDLINE  
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[PMID]: 29380056
[Au] Autor:Naik JS; Walker BR
[Ad] Address:Department of Cell Biology and Physiology, University of New Mexico, MSC08 4750, Albuquerque, NM, 87131, USA. jnaik@salud.unm.edu.
[Ti] Title:Endothelial-dependent dilation following chronic hypoxia involves TRPV4-mediated activation of endothelial BK channels.
[So] Source:Pflugers Arch;, 2018 Jan 29.
[Is] ISSN:1432-2013
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:Following chronic hypoxia (CH), the systemic vasculature exhibits blunted vasoconstriction due to endothelial-dependent hyperpolarization (EDH). Previous data demonstrate that subsequent to CH, EDH-mediated vasodilation switches from a reliance on SK and IK channels to activation of the endothelial BK channels (eBK). The mechanism by which endothelial cell stimulation activates eBK channels following CH is not known. We hypothesized that following CH, EDH-dependent vasodilation involves a TRPV4-dependent activation of eBK channels. ACh induced concentration-dependent dilation in pressurized gracilis arteries from both normoxic and CH rats. Inhibition of TRPV4 (RN-1734) attenuated the ACh response in arteries from CH rats but had no effect in normoxic animals. In the presence of L-NNA and indomethacin, TRPV4 blockade attenuated ACh-induced vasodilation in arteries from CH rats. ACh elicited endothelial TRPV4-mediated Ca events in arteries from both groups. GSK1016790A (GSK101, TRPV4 agonist) elicited vasodilation in arteries from normoxic and CH rats. In arteries from normoxic animals, TRAM-34/apamin abolished the dilation to TRPV4 activation, whereas luminal iberiotoxin had no effect. In CH rats, only administration of all three K channel inhibitors abolished the dilation to TRPV4 activation. Using Duolink®, we observed co-localization between Cav-1, TRPV4, and BK channels in gracilis arteries and in RAECs. Disruption of endothelial caveolae with methyl-ß-cyclodextrin significantly decreased ACh-induced vasodilation in arteries from both groups. In gracilis arteries, endothelial membrane cholesterol was significantly decreased following 48 h of CH. In conclusion, CH results in a functional coupling between muscarinic receptors, TRPV4 and K channels in gracilis arteries.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1007/s00424-018-2112-5

  10 / 41220 MEDLINE  
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[PMID]: 29260240
[Au] Autor:Teixeira JM; Parada CA; Tambeli CH
[Ad] Address:Department of Structural and Functional Biology, Institute of Biology, State University of Campinas, UNICAMP, Rua Monteiro Lobato, 255, Campinas, SP, CEP 13083-862, Brazil.
[Ti] Title:A cyclic pathway of P2 × 7, bradykinin, and dopamine receptor activation induces a sustained articular hyperalgesia in the knee joint of rats.
[So] Source:Inflamm Res;67(4):301-314, 2018 Apr.
[Is] ISSN:1420-908X
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:OBJECTIVE: We investigated whether: (1) P2 × 7 receptor activation by its agonist (BzATP) induces articular hyperalgesia in the rat's knee joint via inflammatory mechanisms and (2) activation of P2 × 7 receptors by endogenous ATP contributes to the articular hyperalgesia induced by bradykinin, TNF-α, IL-1ß, CINC-1, PGE and dopamine. METHODS: The articular hyperalgesia was quantified using the rat knee joint incapacitation test. The knee joint inflammation, characterized by the concentration of pro-inflammatory cytokines and by neutrophil migration, was quantified in the synovial lavage fluid by ELISA and myeloperoxidase enzyme activity assay, respectively. RESULTS: BzATP induced a dose-dependent articular hyperalgesia in the rat's knee joint that was significantly reduced by the selective antagonists for P2 × 7, bradykinin B or B receptors, ß or ß adrenoceptors, and by pre-treatment with Indomethacin. BzATP induced a local increase of TNF-α, IL-1ß, IL-6, and CINC-1 concentration and neutrophil migration into the knee joint. The co-administration of the selective P2 × 7 receptor antagonist A-740003 significantly reduced the articular hyperalgesia induced by bradykinin and dopamine, but not by TNF-α, IL-1ß, CINC-1, and PGE . CONCLUSIONS: P2 × 7 receptor activation induces articular hyperalgesia mediated by the previous inflammatory mediator release. P2 × 7 receptor-induced articular hyperalgesia is sustained by the involvement of this purinergic receptor in bradykinin and dopamine-induced hyperalgesia in the knee joint.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process
[do] DOI:10.1007/s00011-017-1122-7


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