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Article ; Online: In vivo

Aslam, Momna / Feleder, Carlos / Newsom, Ryan J / Campeau, Serge / Musteata, Florin Marcel

Bioanalysis

2019 Volume 11, Issue 16, Page(s) 1523–1534

Abstract: Aim: ...

Abstract	Aim:
MeSH term(s)	Animals ; Brain/metabolism ; Endocannabinoids/isolation & purification ; Endocannabinoids/metabolism ; Humans ; Male ; Rats ; Rats, Sprague-Dawley ; Solid Phase Microextraction/methods ; Stress, Psychological/metabolism
Chemical Substances	Endocannabinoids
Language	English
Publishing date	2019-09-05
Publishing country	England
Document type	Journal Article
ISSN	1757-6199
ISSN (online)	1757-6199
DOI	10.4155/bio-2019-0144
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Article ; Online: The initial fall in arterial pressure evoked by endotoxin is mediated by the ventrolateral periaqueductal gray.

Millington, William R / Yilmaz, M Sertac / Feleder, Carlos

Clinical and experimental pharmacology & physiology

2016 Volume 43, Issue 6, Page(s) 612–615

Abstract: This study tested the hypothesis that the initial fall in arterial pressure evoked by lipopolysaccharide (LPS) is mediated by the ventrolateral column of the midbrain periaqueductal gray region (vlPAG). To test this hypothesis, the local anaesthetic ... ...

Abstract	This study tested the hypothesis that the initial fall in arterial pressure evoked by lipopolysaccharide (LPS) is mediated by the ventrolateral column of the midbrain periaqueductal gray region (vlPAG). To test this hypothesis, the local anaesthetic lidocaine (2%; 0.1 μL, 0.2 μL or 1.0 μL), the delta opioid receptor antagonist naltrindole (2 nmol) or saline was microinjected into the vlPAG of isoflurane-anaesthetized rats bilaterally and LPS (1 mg/kg) or saline was administered intravenously 2 min later. Both lidocaine and naltrindole inhibited LPS-evoked hypotension significantly but did not affect arterial pressure in saline-treated control animals. Neither lidocaine nor naltrindole altered heart rate significantly in either LPS-treated or control animals. Microinjection of lidocaine or naltrindole into the dorsolateral PAG was ineffective. These data indicate that the vlPAG plays an important role in the initiation of endotoxic hypotension and further show that delta opioid receptors in the vlPAG participate in the response.
MeSH term(s)	Animals ; Arterial Pressure/drug effects ; Arterial Pressure/physiology ; Endotoxins/administration & dosage ; Injections, Intraventricular ; Lipopolysaccharides/administration & dosage ; Male ; Periaqueductal Gray/drug effects ; Periaqueductal Gray/physiology ; Rats ; Rats, Sprague-Dawley
Chemical Substances	Endotoxins ; Lipopolysaccharides
Language	English
Publishing date	2016
Publishing country	Australia
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	189277-0
ISSN	1440-1681 ; 0305-1870 ; 0143-9294
ISSN (online)	1440-1681
ISSN	0305-1870 ; 0143-9294
DOI	10.1111/1440-1681.12573
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Article ; Online: Tumor necrosis factor-α induces increased lung vascular permeability: a role for GSK3α/β.

Barton-Pai, Amy / Feleder, Carlos / Johnson, Arnold

European journal of pharmacology

2011 Volume 657, Issue 1-3, Page(s) 159–166

Abstract: We tested the hypothesis that glycogen synthase kinase 3α/β (GSK3α/β) modulates tumor necrosis factor-a (TNF) induced increased lung vascular permeability. Rats were treated with TNF (i.v., ~100ng/ml) or vehicle 0.5h, 4.0h and 24.0h prior to lung ... ...

Abstract	We tested the hypothesis that glycogen synthase kinase 3α/β (GSK3α/β) modulates tumor necrosis factor-a (TNF) induced increased lung vascular permeability. Rats were treated with TNF (i.v., ~100ng/ml) or vehicle 0.5h, 4.0h and 24.0h prior to lung isolation. Rats were co-treated with the GSK3α/β inhibitors SB216763 (0.6mg/kg) or TDZD-8 (1.0mg/kg). After TNF, the isolated lung was assessed for hemodynamics, wet-dry/dry weight (W-D/D) and extravascular albumin. Extravascular albumin significantly increased at TNF-24h compared to Control. In the GSK3α/β-inhibited+TNF groups, extravascular albumin was similar to the Control and respective SB216763 and TDZD-8 groups. In separate studies, to assess GSK3α/β-activity, lung lysate was assessed for phospho-GSK3α/β-Ser(21/9), total GSK3α/β, un-phospho-β-catenin-Ser(33/37) and total β-catenin. In the TNF-4.0h group, there was no change in GSK3α/phospho-GSK3α-Ser(21) but there was an increase in GSK3β/GSK3β-Ser(9) compared to Control, indicating GSK3β activation at TNF-4.0h. GSK3β activation was verified because there was a decrease in un-phospho-β-catenin-Ser(33/37)/β-catenin in the TNF-4.0 group, a specific outcome for GSK3β activation. In the SB216763+TNF group, un-phospho-β-catenin-Ser(33/37) was similar to Control, indicating prevention of TNF-induced GSK3β activation. In the TNF-24h group, there were increases in the biomarkers of inflammation phospho-eNOS-Ser (1117) and oxidized protein, which did not occur in the SB216763+TNF-24h and TDZD-8+TNF-24h groups. In the SB216763+TNF-24h and TDZD-8+TNF-24h groups, un-phospho-β-catenin-Ser(33/37) was greater than in the Control, indicating continued inhibition of GSK3β. The data indicates that pharmacologic inhibition of GSK3β inhibits TNF induced increased endothelial permeability associated with lung inflammation.
MeSH term(s)	Animals ; Biomarkers/metabolism ; Capillary Permeability/drug effects ; Enzyme Activation/drug effects ; Glycogen Synthase Kinase 3/antagonists & inhibitors ; Glycogen Synthase Kinase 3/metabolism ; Glycogen Synthase Kinase 3 beta ; Humans ; Indoles/pharmacology ; Lung/drug effects ; Lung/enzymology ; Lung/metabolism ; Male ; Maleimides/pharmacology ; Nitric Oxide Synthase Type III/metabolism ; Oxidation-Reduction ; Phosphoproteins/chemistry ; Phosphoproteins/metabolism ; Phosphorylation/drug effects ; Protein Kinase Inhibitors/pharmacology ; Rats ; Rats, Sprague-Dawley ; Serine/metabolism ; Thiadiazoles/pharmacology ; Time Factors ; Tumor Necrosis Factor-alpha/pharmacology ; Tyrosine/metabolism ; beta Catenin/chemistry ; beta Catenin/metabolism
Chemical Substances	4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione ; Biomarkers ; Indoles ; Maleimides ; Phosphoproteins ; Protein Kinase Inhibitors ; SB 216763 ; Thiadiazoles ; Tumor Necrosis Factor-alpha ; beta Catenin ; Tyrosine (42HK56048U) ; Serine (452VLY9402) ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; GSK3B protein, human (EC 2.7.11.1) ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; Gsk3b protein, rat (EC 2.7.11.1) ; Glycogen Synthase Kinase 3 (EC 2.7.11.26) ; glycogen synthase kinase 3 alpha (EC 2.7.11.26)
Language	English
Publishing date	2011-02-12
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80121-5
ISSN	1879-0712 ; 0014-2999
ISSN (online)	1879-0712
ISSN	0014-2999
DOI	10.1016/j.ejphar.2011.01.060
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Article ; Online: The OVLT initiates the fall in arterial pressure evoked by high dose lipopolysaccharide: evidence that dichotomous, dose-related mechanisms mediate endotoxic hypotension.

Feleder, Carlos / Sertac Yilmaz, M / Peng, Jianya / Göktalay, Gökhan / Millington, William R

Journal of neuroimmunology

2015 Volume 285, Page(s) 94–100

Abstract: This study tested the hypothesis that lipopolysaccharide (LPS) lowers arterial pressure through two different mechanisms depending on the dose. Previously, we found that a low hypotensive dose of LPS (1mg/kg) lowers arterial pressure by activating vagus ... ...

Abstract	This study tested the hypothesis that lipopolysaccharide (LPS) lowers arterial pressure through two different mechanisms depending on the dose. Previously, we found that a low hypotensive dose of LPS (1mg/kg) lowers arterial pressure by activating vagus nerve afferents. Here we report that hypotension evoked by high dose LPS (15mg/kg) can be prevented by injecting lidocaine into the OVLT but not by vagotomy or inactivation of the NTS. The hypotension produced by both LPS doses was correlated with elevated extracellular norepinephrine concentrations in the POA and prevented by blocking alpha-adrenergic receptors. Thus, initiation of endotoxic hypotension is dose-related, mechanistically.
MeSH term(s)	Animals ; Arterial Pressure/drug effects ; Arterial Pressure/physiology ; Dose-Response Relationship, Drug ; Endotoxemia/chemically induced ; Endotoxemia/physiopathology ; Hypotension/chemically induced ; Hypotension/physiopathology ; Lipopolysaccharides/administration & dosage ; Lipopolysaccharides/toxicity ; Male ; Organum Vasculosum/drug effects ; Organum Vasculosum/physiology ; Rats ; Rats, Sprague-Dawley
Chemical Substances	Lipopolysaccharides
Language	English
Publishing date	2015-08-15
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	8335-5
ISSN	1872-8421 ; 0165-5728
ISSN (online)	1872-8421
ISSN	0165-5728
DOI	10.1016/j.jneuroim.2015.05.023
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Article ; Online: Alterations in affective behavior during the time course of alcohol hangover.

Karadayian, Analía G / Busso, María J / Feleder, Carlos / Cutrera, Rodolfo A

Behavioural brain research

2013 Volume 253, Page(s) 128–138

Abstract: Alcohol hangover is a temporary state described as the unpleasant next-day effects after binge-like drinking. Hangover begins when ethanol is absent in plasma and is characterized by physical and psychological symptoms. Affective behavior is impaired ... ...

Abstract	Alcohol hangover is a temporary state described as the unpleasant next-day effects after binge-like drinking. Hangover begins when ethanol is absent in plasma and is characterized by physical and psychological symptoms. Affective behavior is impaired during the acute phase of alcohol intoxication; however, no reports indicate if similar effects are observed during withdrawal. The aim of this work was to study the time-extension and possible fluctuations in affective behavior during a hangover episode. Male Swiss mice were injected i.p. either with saline (control group) or with ethanol (3.8g/kg BW) (hangover group). Anxiety, fear-related behavior and despair phenotype were evaluated at a basal point (ZT0) and every 2h up to 20h after blood alcohol levels were close to zero (hangover onset). Also, anhedonia signs and pain perception disabilities were studied. Mice exhibited an increase in anxiety-like behavior during 4h and 14h after hangover onset when evaluated by the elevated-plus maze and open field test respectively (p<0.05). Fear-related behavior was detected in hangover animals by the increase of freezing and decrease of line crossings and rearing frequency during 16h after hangover onset (p<0.001). Depression signs were found in hangover mice during 14h (p<0.05). Hangover mice showed a significant decrease in pain perception when tested by tail immersion test at the beginning of hangover (p<0.05). Our findings demonstrate a time-extension between 14 and 16h for hangover affective impairments. This study shows the long lasting effects of hangover over the phase of ethanol intoxication.
MeSH term(s)	Affect/drug effects ; Alcoholic Intoxication/psychology ; Anhedonia ; Animals ; Anxiety/psychology ; Central Nervous System Depressants/adverse effects ; Defecation/physiology ; Ethanol/adverse effects ; Fear/psychology ; Food Preferences ; Hindlimb Suspension/psychology ; Hot Temperature ; Immersion/physiopathology ; Male ; Mice ; Motor Activity/physiology ; Pain Measurement ; Pain Perception/drug effects ; Photic Stimulation ; Sucrose ; Swimming/psychology
Chemical Substances	Central Nervous System Depressants ; Ethanol (3K9958V90M) ; Sucrose (57-50-1)
Language	English
Publishing date	2013-09-15
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	449927-x
ISSN	1872-7549 ; 0166-4328
ISSN (online)	1872-7549
ISSN	0166-4328
DOI	10.1016/j.bbr.2013.07.011
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Article: The preoptic anterior hypothalamic area mediates initiation of the hypotensive response induced by LPS in male rats.

Yilmaz, Mustafa S / Millington, William R / Feleder, Carlos

Shock (Augusta, Ga.)

2008 Volume 29, Issue 2, Page(s) 232–237

Abstract: The mechanism responsible for the initiation of endotoxic hypotension is not fully understood, although it is often attributed to a direct effect of LPS and other vasoactive mediators on the vasculature. Alternatively, recent evidence raises the ... ...

Abstract	The mechanism responsible for the initiation of endotoxic hypotension is not fully understood, although it is often attributed to a direct effect of LPS and other vasoactive mediators on the vasculature. Alternatively, recent evidence raises the possibility that endotoxic hypotension may be initiated through a central mechanism. Previous studies have shown that LPS initiates fever, sickness behavior, and other aspects of the inflammatory response through a neural pathway that sends peripheral inflammatory signals to the preoptic anterior hypothalamic area (POA). It is also well known that the POA plays a role in the regulation of cardiovascular function, but its involvement in LPS-induced hypotension has not been examined previously. Therefore, the aim of the present paper was to investigate whether the initial abrupt fall in arterial pressure evoked by LPS in septic shock is mediated by the POA. LPS (1 mg/kg, i.v.) administration to halothane-anesthetized or conscious rats lowered arterial blood pressure by 24.8+/-2.9 and 25.1+/-5.8 mmHg, respectively. Bilateral lidocaine (2%; 1 microL) injection into the POA, but not the lateral hypothalamus, prevented the hypotension evoked by LPS entirely in both anesthetized and conscious animals. Remarkably, this blockade significantly inhibited the second, delayed fall in arterial pressure induced by LPS, and simultaneously decreased TNF-alpha plasma levels. Together, these data indicate that the initial phase of endotoxic hypotension is mediated by the POA and suggest that the initiation of the hypotensive response induced by LPS can be essential for the development of the late fall in blood pressure.
MeSH term(s)	Animals ; Anterior Hypothalamic Nucleus/drug effects ; Anterior Hypothalamic Nucleus/physiopathology ; Blood Pressure/drug effects ; Hypotension/chemically induced ; Hypotension/physiopathology ; Hypotension/prevention & control ; Lidocaine/pharmacology ; Lipopolysaccharides/toxicity ; Male ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha/blood
Chemical Substances	Lipopolysaccharides ; Tumor Necrosis Factor-alpha ; Lidocaine (98PI200987)
Language	English
Publishing date	2008-02-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1185432-7
ISSN	1540-0514 ; 1073-2322
ISSN (online)	1540-0514
ISSN	1073-2322
DOI	10.1097/shk.0b013e3180caac7e
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Article ; Online: The intracerebroventricular injection of rimonabant inhibits systemic lipopolysaccharide-induced lung inflammation.

Johnson, Arnold / Neumann, Paul H / Peng, Jianya / James, Janey / Russo, Vincenzo / MacDonald, Hunter / Gertzberg, Nancy / Feleder, Carlos

Journal of neuroimmunology

2015 Volume 286, Page(s) 16–24

Abstract: We investigated the role of intracerebroventricular (ICV) injection of rimonabant (500ng), a CB1 antagonist, on lipopolysaccharide ((LPS) 5mg/kg)-induced pulmonary inflammation in rats in an isolated perfused lung model. There were decreases in pulmonary ...

Abstract	We investigated the role of intracerebroventricular (ICV) injection of rimonabant (500ng), a CB1 antagonist, on lipopolysaccharide ((LPS) 5mg/kg)-induced pulmonary inflammation in rats in an isolated perfused lung model. There were decreases in pulmonary capillary pressure (Ppc) and increases in the ((Wet-Dry)/Dry lung weight)/(Ppc) ratio in the ICV-vehicle/LPS group at 4h. There were decreases in TLR4 pathway markers, such as interleukin receptor-associated kinase-1, IκBα, Raf1 and phospho-SFK (Tyr416) at 30min and at 4h increases in IL-6, vascular cell adhesion molecule-1 and myeloperoxidase in lung homogenate. Intracerebroventricular rimonabant attenuated these LPS-induced responses, indicating that ICV rimonabant modulates LPS-initiated pulmonary inflammation.
MeSH term(s)	Animals ; Anti-Inflammatory Agents/administration & dosage ; Cytokines/genetics ; Cytokines/metabolism ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Drug Administration Routes ; Drug Administration Schedule ; Injections, Intraventricular ; Lipopolysaccharides/toxicity ; Lung/drug effects ; Lung/metabolism ; Lung/pathology ; Male ; Peroxidase/metabolism ; Piperidines/administration & dosage ; Pneumonia/chemically induced ; Pneumonia/prevention & control ; Pulmonary Edema/chemically induced ; Pulmonary Edema/prevention & control ; Pyrazoles/administration & dosage ; Rats ; Rats, Sprague-Dawley ; Signal Transduction/drug effects ; Time Factors ; Toll-Like Receptor 4/metabolism
Chemical Substances	Anti-Inflammatory Agents ; Cytokines ; Lipopolysaccharides ; Piperidines ; Pyrazoles ; Tlr4 protein, rat ; Toll-Like Receptor 4 ; Peroxidase (EC 1.11.1.7) ; rimonabant (RML78EN3XE)
Language	English
Publishing date	2015-09-15
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	8335-5
ISSN	1872-8421 ; 0165-5728
ISSN (online)	1872-8421
ISSN	0165-5728
DOI	10.1016/j.jneuroim.2015.07.001
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Article: Preoptic norepinephrine mediates the febrile response of guinea pigs to lipopolysaccharide.

Feleder, Carlos / Perlik, Vit / Blatteis, Clark M

American journal of physiology. Regulatory, integrative and comparative physiology

2007 Volume 293, Issue 3, Page(s) R1135–43

Abstract: Norepinephrine (NE) microdialyzed in the preoptic area (POA) raises core temperature (T(c)) via 1) alpha(1)-adrenoceptors (AR), quickly and independently of POA PGE(2), and 2) alpha(2)-AR, after a delay and PGE(2) dependently. Since systemic ... ...

Abstract	Norepinephrine (NE) microdialyzed in the preoptic area (POA) raises core temperature (T(c)) via 1) alpha(1)-adrenoceptors (AR), quickly and independently of POA PGE(2), and 2) alpha(2)-AR, after a delay and PGE(2) dependently. Since systemic lipopolysaccharide (LPS) activates the central noradrenergic system, we investigated whether preoptic NE mediates LPS fever. We injected LPS (2 microg/kg iv) in guinea pigs prepared with intra-POA microdialysis probes and determined POA cerebrospinal (CSF) NE levels. We similarly microdialyzed prazosin (alpha(1) blocker, 1 microg/microl), yohimbine (alpha(2) blocker, 1 microg/microl), SC-560 [cyclooxygenase (COX)-1 blocker, 5 microg/microl], acetaminophen (presumptive COX-1v blocker, 5 microg/microl), or MK-0663 (COX-2 blocker, 0.5 microg/microl) in other animals before intravenous LPS and measured CSF PGE(2). All of the agents were perfused at 2 microg/min for 6 h. T(c) was monitored constantly. POA NE peaked within 30 min after LPS and then returned to baseline over the next 90 min. T(c) increased within 12 min to a first peak at approximately 60 min and to a second at approximately 150 min and then declined over the following 2.5 h. POA PGE(2) followed a concurrent course. Prazosin pretreatment eliminated the first T(c) rise but not the second; PGE(2) rose normally. Yohimbine pretreatment did not affect the first T(c) rise, which continued unchanged for 6 h; the second rise, however, was absent, and PGE(2) levels did not increase. SC-560 and acetaminophen did not alter the LPS-induced PGE(2) and T(c) rises; MK-0663 prevented both the late PGE(2) and T(c) rises. These results confirm that POA NE is pivotal in the development of LPS fever.
MeSH term(s)	Acetaminophen/pharmacology ; Adrenergic alpha-Antagonists/pharmacology ; Animals ; Body Temperature/physiology ; Catheterization ; Cyclooxygenase Inhibitors/pharmacology ; Dinoprostone/metabolism ; Fever/chemically induced ; Fever/physiopathology ; Guinea Pigs ; Jugular Veins/physiology ; Lipopolysaccharides ; Male ; Microdialysis ; Norepinephrine/physiology ; Prazosin/pharmacology ; Preoptic Area/physiology ; Salmonella enteritidis/chemistry ; Yohimbine/pharmacology
Chemical Substances	Adrenergic alpha-Antagonists ; Cyclooxygenase Inhibitors ; Lipopolysaccharides ; Yohimbine (2Y49VWD90Q) ; Acetaminophen (362O9ITL9D) ; Dinoprostone (K7Q1JQR04M) ; Norepinephrine (X4W3ENH1CV) ; Prazosin (XM03YJ541D)
Language	English
Publishing date	2007-06-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	603839-6
ISSN	1522-1490 ; 0363-6119
ISSN (online)	1522-1490
ISSN	0363-6119
DOI	10.1152/ajpregu.00067.2007
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Article: Preoptic nitric oxide attenuates endotoxic fever in guinea pigs by inhibiting the POA release of norepinephrine.

Feleder, Carlos / Perlik, Vit / Blatteis, Clark M

American journal of physiology. Regulatory, integrative and comparative physiology

2007 Volume 293, Issue 3, Page(s) R1144–51

Abstract: Lipopolysaccharide (LPS) administration induces hypothalamic nitric oxide (NO); NO is antipyretic in the preoptic area (POA), but its mechanism of action is uncertain. LPS also stimulates the release of preoptic norepinephrine (NE), which mediates fever ... ...

Abstract	Lipopolysaccharide (LPS) administration induces hypothalamic nitric oxide (NO); NO is antipyretic in the preoptic area (POA), but its mechanism of action is uncertain. LPS also stimulates the release of preoptic norepinephrine (NE), which mediates fever onset. Because NE upregulates NO synthases and NO induces cyclooxygenase (COX)-2-dependent PGE(2), we investigated whether NO mediates the production of this central fever mediator. Conscious guinea pigs with intra-POA microdialysis probes received LPS intravenously (2 mug/kg) and, thereafter, an NO donor (SIN-1) or scavenger (carboxy-PTIO) intra-POA (20 mug/mul each, 2 mul/min, 6 h). Core temperature (T(c)) was monitored constantly; dialysate NE and PGE(2) were analyzed in 30-min collections. To verify the reported involvement of alpha(2)-adrenoceptors (AR) in PGE(2) production, clonidine (alpha(2)-AR agonist, 2 mug/mul) was microdialyzed with and without SIN-1 or carboxy-PTIO. To assess the possible involvement of oxidative NE and/or NO products in the demonstrated initially COX-2-independent POA PGE(2) increase, (+)-catechin (an antioxidant, 3 mug/mul) was microdialyzed, and POA PGE(2), and T(c) were determined. SIN-1 and carboxy-PTIO reduced and enhanced, respectively, the rises in NE, PGE(2), and T(c) produced by intravenous LPS. Similarly, they prevented and increased, respectively, the delayed elevations of PGE(2) and T(c) induced by intra-POA clonidine. (+)-Catechin prevented the LPS-induced elevation of PGE(2), but not of T(c). We conclude that the antipyretic activity of NO derives from its inhibitory modulation of the LPS-induced release of POA NE. These data also implicate free radicals in POA PGE(2) production and raise questions about its role as a central LPS fever mediator.
MeSH term(s)	Acetaminophen/pharmacology ; Adrenergic alpha-Antagonists/pharmacology ; Animals ; Body Temperature/physiology ; Catheterization ; Cyclooxygenase Inhibitors/pharmacology ; Dinoprostone/metabolism ; Fever/chemically induced ; Fever/physiopathology ; Guinea Pigs ; Jugular Veins/physiology ; Lipopolysaccharides ; Male ; Microdialysis ; Norepinephrine/physiology ; Prazosin/pharmacology ; Preoptic Area/physiology ; Salmonella enteritidis/chemistry ; Yohimbine/pharmacology
Chemical Substances	Adrenergic alpha-Antagonists ; Cyclooxygenase Inhibitors ; Lipopolysaccharides ; Yohimbine (2Y49VWD90Q) ; Acetaminophen (362O9ITL9D) ; Dinoprostone (K7Q1JQR04M) ; Norepinephrine (X4W3ENH1CV) ; Prazosin (XM03YJ541D)
Language	English
Publishing date	2007-06-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	603839-6
ISSN	1522-1490 ; 0363-6119
ISSN (online)	1522-1490
ISSN	0363-6119
DOI	10.1152/ajpregu.00068.2007
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Article ; Online: Inhibition of monosodium urate crystal-induced inflammation by scopoletin and underlying mechanisms.

Yao, Xiujuan / Ding, Zuoqi / Xia, Yufeng / Wei, Zhifeng / Luo, Yubin / Feleder, Carlos / Dai, Yue

International immunopharmacology

2012 Volume 14, Issue 4, Page(s) 454–462

Abstract: The present study determined the anti-inflammatory activity of scopoletin in gout air pouch model and revealed the underlying mechanisms by in vitro assays. Monosodium urate (MSU) crystal-induced inflammation in mouse air pouch model, an experimental ... ...

Abstract	The present study determined the anti-inflammatory activity of scopoletin in gout air pouch model and revealed the underlying mechanisms by in vitro assays. Monosodium urate (MSU) crystal-induced inflammation in mouse air pouch model, an experimental model for acute gout, was used to assess the efficacy of scopoletin. The neutrophil and mononuclear phagocyte numbers and MPO levels were increased significantly six hours after MSU crystal injection into the air pouch, whereas these changes were inhibited substantially upon scopoletin (100 and 200mg/kg, i.p.) treatment. To get insight into the underlying mechanisms, the in vitro studies were performed to investigate the effects of scopoletin on activation of macrophages and resultant production of inflammatory mediators. The secretions of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), prostaglandin E(2) (PGE(2)) and nitric oxide (NO) were elevated in MSU crystal-stimulated RAW 264.7 cells, and scopoletin (30-300 μM) suppressed the production of all mediators. Moreover, RT-PCR assay and western blot analysis indicated that scopoletin regulated the transcriptional level of these mediators via suppression of NF-κB activation and blockade of MAPK signal pathway. Thus, the results clearly indicated that scopoletin inhibited the monosodium urate crystal-induced inflammation both in vivo and in vitro. In combination with our previous findings that scopoletin shows hypouricemic, anti-angiogenesis and pro-apoptotic activities, this compound may be a potential agent for gout therapy and could serve as a structural base for developing new drugs.
MeSH term(s)	Animals ; Cell Line ; Cell Survival ; Cytokines/genetics ; Cytokines/metabolism ; Gene Expression Regulation/drug effects ; Humidity ; Inflammation/chemically induced ; Inflammation/drug therapy ; Leukocytes ; Macrophages ; Male ; Mice ; Mice, Inbred ICR ; Molecular Structure ; Nitric Oxide/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Scopoletin/chemistry ; Scopoletin/pharmacology ; Temperature ; Uric Acid/toxicity
Chemical Substances	Cytokines ; RNA, Messenger ; Uric Acid (268B43MJ25) ; Nitric Oxide (31C4KY9ESH) ; Scopoletin (KLF1HS0SXJ)
Language	English
Publishing date	2012-12
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2043785-7
ISSN	1878-1705 ; 1567-5769
ISSN (online)	1878-1705
ISSN	1567-5769
DOI	10.1016/j.intimp.2012.07.024
Database	MEDical Literature Analysis and Retrieval System OnLINE

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