The Experts below are selected from a list of 9651 Experts worldwide ranked by ideXlab platform
Mahmoud M Khattab - One of the best experts on this subject based on the ideXlab platform.
-
tempol a membrane permeable radical scavenger attenuates peroxynitrite and superoxide anion enhanced carrageenan induced Paw Edema and hyperalgesia a key role for superoxide anion
European Journal of Pharmacology, 2006Co-Authors: Mahmoud M KhattabAbstract:Abstract Carrageenan produces both inflammation and pain when injected in rat Paws via enhancement of the formation of reactive oxygen species. We have tested the effect of 4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl (TEMPOL), a membrane-permeable superoxide dismutase (SOD) mimetic in Carrageenan-Induced rat Paw Edema. Treatment of rats with TEMPOL (15, 30, and 60 mg/kg, 15 min prior to carrageenan) inhibited the Paw Edema. Furthermore, treatment of rats with the SOD inhibitor diethylthiocarbamate (DETCA, 100 mg/kg, 1 h before carrageenan) enhanced the Carrageenan-Induced Paw Edema. Co-administration of peroxynitrite with carrageenan produced a similar fortification of the Carrageenan-Induced Edema. Prior treatment of rats with TEMPOL (30 mg/kg) inhibited the enhancement produced by DETCA treatment (endogenous superoxide anion stress) as well as that produced by the peroxynitrite stress. The effect of TEMPOL as well as the influence of superoxide anion and peroxynitrite stresses was also tested in Carrageenan-Induced hyperalgesia model. Carrageenan (500 μg/Paw) produced significant hyperalgesia presented as shortening of withdrawal latency times using hot plate (52 °C) starting 30 min after carrageenan and lasting for 3 h. TEMPOL (60 mg/kg, injected 15 min before carrageenan) ameliorated this hyperalgesia during the first 2 h. Concurrent administration of peroxynitrite promptly intensified the carrageenan hyperalgesia. TEMPOL (60 mg/kg, 15 min before peroxynitrite–carrageenan) inhibited the peroxynitrite enhancement of carrageenan hyperalgesia when tested at 60 min after injection of the cocktail. The present investigation gives the proof for the effectiveness of TEMPOL as anti-inflammation and analgesic agents in Carrageenan-Induced model of inflammation and hyperalgesia. It further indicated the importance of superoxide anion and peroxynitrite in acute inflammation and inflammatory pain. This raises the chances for considering pharmacologic interventions that interrupt superoxide anion and peroxynitrite stress for putative alternative agents as anti-inflammatory analgesic new medical strategies.
-
TEMPOL, a membrane-permeable radical scavenger, attenuates peroxynitrite- and superoxide anion-enhanced Carrageenan-Induced Paw Edema and hyperalgesia: a key role for superoxide anion.
European journal of pharmacology, 2006Co-Authors: Mahmoud M KhattabAbstract:Carrageenan produces both inflammation and pain when injected in rat Paws via enhancement of the formation of reactive oxygen species. We have tested the effect of 4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl (TEMPOL), a membrane-permeable superoxide dismutase (SOD) mimetic in Carrageenan-Induced rat Paw Edema. Treatment of rats with TEMPOL (15, 30, and 60 mg/kg, 15 min prior to carrageenan) inhibited the Paw Edema. Furthermore, treatment of rats with the SOD inhibitor diethylthiocarbamate (DETCA, 100 mg/kg, 1 h before carrageenan) enhanced the Carrageenan-Induced Paw Edema. Co-administration of peroxynitrite with carrageenan produced a similar fortification of the Carrageenan-Induced Edema. Prior treatment of rats with TEMPOL (30 mg/kg) inhibited the enhancement produced by DETCA treatment (endogenous superoxide anion stress) as well as that produced by the peroxynitrite stress. The effect of TEMPOL as well as the influence of superoxide anion and peroxynitrite stresses was also tested in Carrageenan-Induced hyperalgesia model. Carrageenan (500 mug/Paw) produced significant hyperalgesia presented as shortening of withdrawal latency times using hot plate (52 degrees C) starting 30 min after carrageenan and lasting for 3 h. TEMPOL (60 mg/kg, injected 15 min before carrageenan) ameliorated this hyperalgesia during the first 2 h. Concurrent administration of peroxynitrite promptly intensified the carrageenan hyperalgesia. TEMPOL (60 mg/kg, 15 min before peroxynitrite-carrageenan) inhibited the peroxynitrite enhancement of carrageenan hyperalgesia when tested at 60 min after injection of the cocktail. The present investigation gives the proof for the effectiveness of TEMPOL as anti-inflammation and analgesic agents in Carrageenan-Induced model of inflammation and hyperalgesia. It further indicated the importance of superoxide anion and peroxynitrite in acute inflammation and inflammatory pain. This raises the chances for considering pharmacologic interventions that interrupt superoxide anion and peroxynitrite stress for putative alternative agents as anti-inflammatory analgesic new medical strategies.
Daniele Piomelli - One of the best experts on this subject based on the ideXlab platform.
-
Acute Intracerebroventricular Administration of Palmitoylethanolamide, an Endogenous Peroxisome Proliferator-Activated Receptor-α Agonist, Modulates Carrageenan-Induced Paw Edema in Mice
The Journal of pharmacology and experimental therapeutics, 2007Co-Authors: Giuseppe D'agostino, Giovanna La Rana, Roberto Russo, Oscar Sasso, Anna Iacono, Emanuela Esposito, Giuseppina Mattace Raso, Salvatore Cuzzocrea, Jesse Lo Verme, Daniele PiomelliAbstract:Peroxisome proliferator-activated receptor (PPAR)-alpha is a nuclear transcription factor. Although the presence of this receptor in different areas of central nervous system (CNS) has been reported, its role remains unclear. Palmitoylethanolamide (PEA), a member of the fatty-acid ethanolamide family, acts peripherally as an endogenous PPAR-alpha ligand, exerting analgesic and anti-inflammatory effects. High levels of PEA in the CNS have been found, but the specific function of this lipid remains to be clarified. Using Carrageenan-Induced Paw Edema in mice, we show that i.c.v. administration of PEA may control peripheral inflammation through central PPAR-alpha activation. A single i.c.v. administration of 0.01 to 1 microg of PEA, 30 min before carrageenan injection, reduced Edema formation in the mouse carrageenan test. This effect was mimicked by 0.01 to 1 microg of GW7647 [2-[[4-[2-[[(cyclohexylamino)carbonyl](4-cyclohexylbutyl)amino]ethyl]phenyl]thio]-2-methylpropanoic acid], a synthetic PPAR-alpha agonist. Moreover, central PEA administration significantly reduced the expression of the proinflammatory enzymes cyclooxygenase-2 and inducible nitric-oxide synthase, and it significantly restored Carrageenan-Induced PPAR-alpha reduction in the spinal cord. To investigate the mechanism by which i.c.v. PEA attenuated the development of Carrageenan-Induced Paw Edema, we evaluated inhibitor kappaB-alpha (I kappa B-alpha) degradation and nuclear factor-kappaB (NF-kappaB) p65 activation in the cytosolic or nuclear extracts from spinal cord tissue. PEA prevented IkB-alpha degradation and NF-kappaB nuclear translocation, confirming the involvement of this transcriptional factor in the control of peripheral inflammation. The obligatory role of PPAR-alpha in mediating the effects of PEA was confirmed by the lack of the compounds anti-inflammatory effects in mutant mice lacking PPAR-alpha. In conclusion, our data show for the first time that PPAR-alpha activation in the CNS can control peripheral inflammation.
Halis Suleyman - One of the best experts on this subject based on the ideXlab platform.
-
The effects of 3-benzoyl-1-methyl-4-phenyl-4 piperidinolhydrochloride (C1), indomethacin, nimesulide and rofecoxib on cyclooxygenase activities in Carrageenan-Induced Paw Edema model
Turkish Journal of Medical Sciences, 2010Co-Authors: Yaşar Nuri Şahin, Halis Suleyman, Berna Demircan, Hülya Aksoy, Halise Inci GulAbstract:Aim: The aim of this study was to investigate the effects of 3-benzoyl-1-methyl-4-phenyl-4-piperidinol-hydrochloride (C1), which is a structural and also non-classical isomer of bis Mannich base, bis (3-aryl-3-oxo-propyl) methylamine hydrochlorides (B1), on cyclooxygenase (COX) activities in 48 rats with inflammation by using Carrageenan-Induced Paw Edema, and to compare its effect with other non-steroidal anti-inflammatory drugs (NSAIDs). Materials and methods: Experimental animals were supplied by the Center of Experimental Research and Practice in Ataturk University. The animals were housed and fed in the laboratory (normal room temparature, food and water) under standard conditions. Rats were randomly assigned to eight groups (n = 6); control, intact, indomethacin, nimesulide, rofecoxib, C1 (50 mg), C1 (100 mg), and C1(200 mg). Results: C1 significantly inhibited COX-1 (P < 0.01 for all) and COX-2 (P < 0.01 for all) activities at the doses of 50, 100, and 200 mg kg −1 when compared to control group. The inhibitory effect of C1 on COX-1 and COX-2 activities at all doses was similar to those of nimesulide. While C1 at 200 mg kg −1 significantly inhibited COX-1 and COX-2 activities (P < 0.01 for both), at C1 100 mg kg −1 significantly inhibited only COX-1 activity in comparison to rofecoxib (P < 0.05). Inhibitory effects of C1 on COX-1 activity at the doses of 50 and 100 mg kg −1 were significantly weaker when compared to indomethacin (P < 0.01 and P < 0.05, respectively). Conclusion: It may be claimed that C1 has an anti-inflammatory effect, and its COX-2 selectivity is stronger than indomethacin and nimesulide but weaker than rofecoxib.
-
amiodarone has anti inflammatory and anti oxidative properties an experimental study in rats with carrageenan induced Paw Edema
European Journal of Pharmacology, 2007Co-Authors: Zekai Halici, Gunnur Ozbakis Dengiz, Fehmi Odabasoglu, Elif Cadirci, Halis Suleyman, Mesut HaliciAbstract:Abstract Amiodarone is a widely used anti-arrhythmic agent. We have investigated alterations in the glutathione (GSH) level and the activities of anti-oxidative enzymes (superoxide dismutase, catalase, glutathione s-transferase and glutathione reductase) and myeloperoxidase, as marker of acute inflammation, following oral administration of amiodarone and diclofenac in rats with Carrageenan-Induced Paw Edema. In the present study, we found that 1) Amiodarone reduced the development of Carrageenan-Induced Paw Edema, to a greater degree than diclofenac; 2) Amiodarone and diclofenac alleviated increases in the activities of catalase and glutathione s-transferase enzymes resulting from Edema; 3) Amiodarone and diclofenac ameliorated depressions in the GSH level and the activities of superoxide dismutase and glutathione reductase enzymes caused by carrageenan injection; and 4) All doses of amiodarone and diclofenac caused an amplification in myeloperoxidase activity resulting from induced Paw Edema. These results suggest that the anti-inflammatory effect of amiodarone on Carrageenan-Induced acute inflammation can be attributed to its ameliorating effect on the oxidative damage.
-
Beneficial interaction of nimesulide with NSAIDs
Medicinal Chemistry Research, 2007Co-Authors: Halis Suleyman, Elif Cadirci, Emine Salamci, Zekai HaliciAbstract:In this study, the effects of nimesulide on the antiinflammatory and ulcerative action of some nonsteroidal antiinflammatory drugs (NSAIDs; (diclofenac sodium, ibuprofen, meloxicam) were investigated in rats, and it was determined whether nimesulide interacts with these drugs in vivo and in vitro. Results showed that while diclofenac sodium, ibuprofen, and meloxicam reduced Carrageenan-Induced Paw Edema in rats by 66%, 39.6%, and 58%, respectively, when used alone, they reduced Carrageenan-Induced Paw Edema by 69.8%, 56.6%, and 66%, respectively, when combined with nimesulide. Diclofenac (25 mg kg-1) and meloxicam (7.5 mg kg-1) produced 9.3 and 19.6 mm2 ulcer areas in stomachs of rats, respectively, when used alone, but when combined with nimesulide diclofenac and meloxicam did not cause any injury in rat stomachs. While ranitidine at 100 mg kg-1 dose prevented diclofenac-induced ulcer formation, it reduced meloxicam-induced ulcer formation significantly. We conclude that nimesulide does not interact with these drugs in terms of antiinflammatory action and antagonizes their side effects on gastric tissue without reacting chemically.
-
Anti-inflammatory activity of 3-benzoyl-1-methyl-4-phenyl-4-piperidinol hydrochloride.
Pharmacological research, 2003Co-Authors: Halis Suleyman, Halise Inci Gul, Mehmet AsogluAbstract:In our study, the effects of the compound 3-benzoyl-1-methyl-4-phenyl-4-piperidinol hydrochloride (C1) and also an anti-inflammatory drug, indomethacin, tested by Carrageenan-Induced Paw Edema and cotton pellet granuloma tests, for their effects on acute and chronic phases of inflammation, respectively. Their effects on vascular permeability were also tested by hyaluronidase-induced capillary permeability. C1 decreased the Carrageenan-Induced Paw Edema 61.98, 80.84, and 90.32% at 50, 100, and 200mgkg(-1) doses, respectively, while this decrease was 89.93% by indomethacin at 20mgkg(-1) dose. Antiproliferative effects of C1 at 100mgkg(-1) and indomethacinin at 20mgkg(-1) doses were 46.1 and 43.1%, respectively, in cotton pellet test. C1 and indomethacin both significantly inhibited the hyaluronidase-induced increase in capillary permeability.
-
The effects of newly synthesized pyrazole derivatives on formaldehyde-, carrageenan-, and dextran-induced acute Paw Edema in rats.
Biological & Pharmaceutical Bulletin, 2001Co-Authors: Halis Suleyman, Mehmet Emin BuyukokurogluAbstract:The antiinflammatory effects of 10 newly synthesized pyrazole derivatives on formaldehyde-induced rat Paw Edema were investigated. The most effective of them (K-3) was investigated again in dextran- and Carrageenan-Induced Paw Edema. In formaldehyde-induced Paw Edema, K-3 50, 100, and 200 mg/kg p.o. inhibited the Edema by 48.9% (p
Ardeshir Talebi - One of the best experts on this subject based on the ideXlab platform.
-
further studies on anti inflammatory activity of maprotiline in carrageenan induced Paw Edema in rat
International Immunopharmacology, 2013Co-Authors: Hossein Sadeghi, Valiolla Hajhashemi, Mohsen Minaiyan, Ahmad Movahedian, Ardeshir TalebiAbstract:Abstract Antidepressant drugs are commonly used for treatment of different medical disorders besides of psychiatric diseases. Accumulating evidence suggests that antidepressants exhibit anti-inflammatory activity in vivo and in vitro conditions, but the mechanisms of this property are not clear very well. In our earlier work, we demonstrated that i.c.v. and i.p. injection of maprotiline, as an antidepressant, decreased Paw Edema at the fourth hour after subplantar injection of carrageenan. Therefore, this work was undertaken to investigate anti-inflammatory effects of maprotiline in more details. Our results verified that i.p. (25 and 50 mg/kg) and i.c.v. (100 μg/rat) application of maprotiline significantly reduced Paw Edema at 1, 2, 3 and 4 h intervals after carrageenan challenge. Pathological examinations and MPO activity also showed that both i.p. and i.c.v. maprotiline considerably inhibited infiltration of PMN leucocytes into the inflamed Paws. Additionally, i.p. and i.c.v. maprotiline at all applied doses noticeably declined levels of IL-1β into the site of inflammation, while only i.p. maprotiline at a dose of 50 mg/kg significantly decreased TNF-α levels in the carrageenan-injected Paws. These results confirmed anti-Edematogenic activity of i.p. and i.c.v. maprotiline in the carrageenan induced Paw Edema model and showed that these properties of maprotiline might be mediated through inhibition of PMN infiltration and release of IL-1β and TNF-α.
-
A study on the mechanisms involving the anti-inflammatory effect of amitriptyline in Carrageenan-Induced Paw Edema in rats.
European Journal of Pharmacology, 2011Co-Authors: Hossein Sadeghi, Valiolla Hajhashemi, Mohsen Minaiyan, Ahmad Movahedian, Ardeshir TalebiAbstract:Anti-inflammatory effects of antidepressants have been reported in some studies, but the mechanisms underlying these effects remain unknown. Amitriptyline, a tricyclic antidepressant, is widely used in the management of psychological disorders and various types of pain, including neuropathic pain or fibromyalgia. In our previous work, we found the role of supraspinal mechanisms in the anti-inflammatory effect of amitriptyline. In the line of the indicated study, we sought to evaluate the effects of intraperitoneal (i.p.) and intracerebroventricular (i.c.v.) application of amitriptyline in the Carrageenan-Induced Paw Edema in rats in more details. Our findings confirmed that i.p. (40 and 80 mg/kg) and i.c.v. (100 μg/rat) injection of amitriptyline inhibited Carrageenan-Induced inflammation at different times. We also found that both i.p. and i.c.v. amitriptyline significantly decreased migration of polymorphonuclear (PMN) leucocytes into the site of inflammation, according to pathological evidence and the activity of myeloperoxidase (MPO). Furthermore, i.p. amitriptyline at the applied doses markedly reduced interleukin (IL)-1β and tumor necrosis factor (TNF)-α levels in the Paw treated with carrageenan. Our results also showed that i.c.v. amitriptyline noticeably decreased the concentration of IL-1β in the inflamed Paws. The TNF-α levels reduced in the i.c.v. group, even though these reductions were not statistically significant. These results confirmed the anti-inflammatory effects of systemic and central amitriptyline in the Carrageenan-Induced Paw Edema in rats, and demonstrated that these effects mediated mostly through the inhibition of PMN cells migration and release of IL-1β and TNF-α into the site of inflammation.
-
effect of fluvoxamine on carrageenan induced Paw Edema in rats evaluation of the action sites
Iranian Journal of Pharmaceutical Research, 2011Co-Authors: Valiolla Hajhashemi, Mohsen Minaiyan, Ahmad Movahedian, Hossein Sadeghi, Ardeshir TalebiAbstract:The present study was designed to explore the anti-inflammatory effect of fluvoxamine, as a selective serotonin reuptake inhibitor (SSRI) anti-depressant, on Carrageenan-Induced Paw Edema in more details. At first, fluvoxamine was administered intra-peritoneally (2.5, 12.5, 25 and 50 mg Kg -1 ) 30 min before the subplantar injection of carrageenan. Fluvoxamine was also injected intra-peritoneally at a dose of 50 mg Kg -1 30 or 90 min after carrageenan injection. Then, fluvoxamine was given intra-cerebroventricularly (25, 50 and 100 μg/rat) and intrathecally (25, 50 and 100 μg/rat) 30 min before the carrageenan challenge. Finally, the effect of mifepristone (5 mg Kg -1 ), an antagonist of the glucocorticoid receptor, on the anti-Edema effect of fluvoxamine (50 mg Kg -1 ) was investigated. Results showed that intra-peritoneal (IP) administration of fluvoxamine before or after carrageenan injection considerably inhibited Paw Edema response at 4 h post-carrageenan (p < 0.001), but intra-cerebroventricular (i.c.v.) and intra-thecal (i.t.) injection of fluvoxamine did not alter the degree of Paw swelling. The inhibitory effect of fluvoxamine was reduced by the pretreatment of mifepristone (p < 0.01). Our results suggest that IP administration of fluvoxamine produces a noticeable antiinflammatory effect in the Carrageenan-Induced Paw Edema in rats and at least, a part of this effect is mediated through glucocorticoid receptor. Moreover, it seems unlikely that central sites have an important role in this inhibitory effect of fluvoxamine.
-
central and peripheral anti inflammatory effects of maprotiline on carrageenan induced Paw Edema in rats
Inflammation Research, 2010Co-Authors: Valiolla Hajhashemi, Hojjat Sadeghi, Mohsen Minaiyan, Ahmad Movahedian, Ardeshir TalebiAbstract:Objective To explore the site of action of maprotiline, as an atypical antidepressant, on Carrageenan-Induced Paw Edema.
-
the role of central mechanisms in the anti inflammatory effect of amitriptyline on carrageenan induced Paw Edema in rats
Clinics, 2010Co-Authors: Valiolla Hajhashemi, Mohsen Minaiyan, Ahmad Movahedian, Hossein Sadeghi, Ardeshir TalebiAbstract:OBJECTIVE: The present study was designed to further investigate the effect of amitriptyline, a classical tricyclic antidepressant, on Carrageenan-Induced Paw Edema in rats. METHODS: First, amitriptyline was administered intraperitoneally (i.p.) at doses of 20, 40 and 80 mg kg-1, 30 min before subplantar injection of carrageenan. Second, amitriptyline was given intracerebroventriculary or intrathecally at doses of 25, 50 and 100 μg/rat, 30 min prior to carrageenan challenge. Third, the effect of adrenergic receptor antagonists such as propranolol (10 mg kg-1, i.p.), prazosin (4 mg kg-1, i.p.) and yohimbine (10 mg kg-1, i.p.) and an opioid receptor antagonist (naloxone, 4 mg kg-1, i.p.) on the anti-inflammatory effect of amitriptyline (40 mg kg-1, i.p.) was investigated. RESULTS: Our data confirm that intraperitoneally administered amitriptyline exhibits a marked anti-inflammatory effect on Carrageenan-Induced Paw Edema in rats 4 h postcarrageenan challenge (P < 0.001). Intracerebroventricular (i.c.v.) administration of amitriptyline also reduced the development of Paw Edema at 4 h postcarrageenan (P < 0.001), but intrathecal (i.t.) application of amitriptyline failed to alter the degree of Paw swelling. Furthermore, the applied antagonists did not modify the anti-inflammatory effect of amitriptyline. CONCLUSION: These results support the view that amitriptyline has a considerable anti-inflammatory effect on Carrageenan-Induced Paw Edema in rats and suggest that at least a part of this property could be mediated through supraspinal sites. Moreover, it seems unlikely that the investigated adrenergic and opioid receptors have a significant role in this effect of amitriptyline.
Valiolla Hajhashemi - One of the best experts on this subject based on the ideXlab platform.
-
maprotiline inhibits cox2 and inos gene expression in lipopolysaccharide stimulated u937 macrophages and carrageenan induced Paw Edema in rats
Central European Journal of Immunology, 2019Co-Authors: Laleh Rafiee, Valiolla Hajhashemi, Shaghayegh Haghjooy JavanmardAbstract:Maprotiline, a tetracyclic antidepressant, is used for the management of mental disorders and various types of chronic pain. In our previous work, we found the inhibitory effect of maprotiline on inflammatory mediator's expression like tumor necrosis factor α (TNF-α and interleukin 1β (IL-1β. As part of that study, we sought to evaluate the effect of maprotiline on the expression of some inflammatory mediators such as cyclooxygenases 2 (COX2) and inducible nitric oxide synthase (iNOS). For this reason we used an in vitro model system of lipopolysaccharide (LPS)-stimulated human U937 macrophages and also an in vivo model of Carrageenan-Induced Paw Edema in rats. We measured the expression of these genes by quantitative RT-real time PCR. The expression of COX2 and iNOS significantly decreased by maprotiline in U937 macrophages and Carrageenan-Induced Paw inflammation in rats. Our finding also confirmed that intraperitoneal (i.p.) injection of maprotiline inhibited Carrageenan-Induced Paw Edema. Moreover, maprotiline significantly decreased the migration of polymorphonuclear (PMN) leukocytes to the site of inflammation. The results of the present study provide further evidence for the anti-inflammatory effect of maprotiline. This effect appears to be mediated by down regulation of inflammatory genes. Further studies are needed to evaluate the complex cellular and molecular mechanisms of maprotiline.
-
Fluvoxamine inhibits some inflammatory genes expression in LPS/stimulated human endothelial cells, U937 macrophages, and Carrageenan-Induced Paw Edema in rat.
Iranian Journal of Basic Medical Sciences, 2016Co-Authors: Laleh Rafiee, Valiolla Hajhashemi, Shaghayegh Haghjooy JavanmardAbstract:Objective(s): Fluvoxamine is a well-known selective serotonin reuptake inhibitor (SSRI); Despite its anti-inflammatory effect, little is known about the precise mechanisms involved. In our previous work, we found that IP administration of fluvoxamine produced a noticeable anti-inflammatory effect in Carrageenan-Induced Paw Edema in rats. In this study, we aimed to evaluate the effect of fluvoxamine on the expression of some inflammatory genes like intercellular adhesion molecule (ICAM1), vascular cell adhesion molecule (VCAM1), cyclooxygenases2 (COX2), and inducible nitric oxide synthase (iNOS). Materials and Methods: An in vitro model of LPS stimulated human endothelial cells and U937 macrophages were used. Cells were pretreated with various concentrations of fluvoxamine, from 10-8 M to 10-6 M. For in vivo model, fluvoxamine was administered IP at doses of 25 and 50 mg/kg-1, before injection of carrageenan. At the end of experiment, the expression of mentioned genes were measured by quantitative real time (RT)-PCR in cells and in Paw Edema in rat. Results: The expression of ICAM1, VCAM1, COX2, and iNOS was significantly decreased by fluvoxamine in endothelial cells, macrophages, and in rat Carrageenan-Induced Paw Edema. Our finding also confirmed that IP injection of fluvoxamine inhibits Carrageenan-Induced inflammation in rat Paw Edema. Conclusion: The results of present study provide further evidence for the anti-inflammatory effect of fluvoxamine. This effect appears to be mediated by down regulation of inflammatory genes. Further studies are needed to evaluate the complex cellular and molecular mechanisms of immunomodulatory effect of fluvoxamine.
-
the anti inflammatory effects of venlafaxine in the rat model of carrageenan induced Paw Edema
Iranian Journal of Basic Medical Sciences, 2015Co-Authors: Valiolla Hajhashemi, Mohsen Minaiyan, Azam Mesdaghinia, Hamid Reza Banafshe, Alireza AbedAbstract:OBJECTIVES: Recently anti-inflammatory effects of antidepressants have been demonstrated. Venlafaxine belongs to newer antidepressants with serotonin norepinephrine reuptake inhibition property. The pain alleviating properties of venlafaxine in different pain models such as neurogenic pain, diabetic neuropathy, and fibromyalgia have been demonstrated. Anti-inflammatory effects of venlafaxine and also its underlying mechanisms remain unclear. The present study was designed to evaluate the anti-inflammatory effects of venlafaxine and determine possible underlying mechanisms. MATERIALS AND METHODS: We examined the anti-inflammatory effects of intraperitoneal (IP) and intracerebroventricular (ICV) administration of venlafaxine in the rat model of Carrageenan-Induced Paw Edema. RESULTS: Our results showed that both IP (50 and 100 mg/kg) and ICV (50 and 100 μg/rat) injection of venlafaxine inhibited Carrageenan-Induced Paw Edema. Also IP and ICV administration of venlafaxine significantly decreased myeloperoxidase (MPO) activity and interleukin (IL)-1β and tumor necrosis factor (TNF)-α production. Finally, we tried to reverse the anti-inflammatory effect of venlafaxine by yohimbine (5 mg/kg, IP), an alpha2-adrenergic antagonist. Our results showed that applied antagonist failed to change the anti-inflammatory effect of venlafaxine. CONCLUSION: These results demonstrated that venlafaxine has potent anti-inflammatory effect which is related to the peripheral and central effects of this drug. Also we have shown that anti-inflammatory effect of venlafaxine is mediated mostly through the inhibition of IL-1β and TNF-α production and decreases MPO activity in the site of inflammation.
-
further studies on anti inflammatory activity of maprotiline in carrageenan induced Paw Edema in rat
International Immunopharmacology, 2013Co-Authors: Hossein Sadeghi, Valiolla Hajhashemi, Mohsen Minaiyan, Ahmad Movahedian, Ardeshir TalebiAbstract:Abstract Antidepressant drugs are commonly used for treatment of different medical disorders besides of psychiatric diseases. Accumulating evidence suggests that antidepressants exhibit anti-inflammatory activity in vivo and in vitro conditions, but the mechanisms of this property are not clear very well. In our earlier work, we demonstrated that i.c.v. and i.p. injection of maprotiline, as an antidepressant, decreased Paw Edema at the fourth hour after subplantar injection of carrageenan. Therefore, this work was undertaken to investigate anti-inflammatory effects of maprotiline in more details. Our results verified that i.p. (25 and 50 mg/kg) and i.c.v. (100 μg/rat) application of maprotiline significantly reduced Paw Edema at 1, 2, 3 and 4 h intervals after carrageenan challenge. Pathological examinations and MPO activity also showed that both i.p. and i.c.v. maprotiline considerably inhibited infiltration of PMN leucocytes into the inflamed Paws. Additionally, i.p. and i.c.v. maprotiline at all applied doses noticeably declined levels of IL-1β into the site of inflammation, while only i.p. maprotiline at a dose of 50 mg/kg significantly decreased TNF-α levels in the carrageenan-injected Paws. These results confirmed anti-Edematogenic activity of i.p. and i.c.v. maprotiline in the carrageenan induced Paw Edema model and showed that these properties of maprotiline might be mediated through inhibition of PMN infiltration and release of IL-1β and TNF-α.
-
A study on the mechanisms involving the anti-inflammatory effect of amitriptyline in Carrageenan-Induced Paw Edema in rats.
European Journal of Pharmacology, 2011Co-Authors: Hossein Sadeghi, Valiolla Hajhashemi, Mohsen Minaiyan, Ahmad Movahedian, Ardeshir TalebiAbstract:Anti-inflammatory effects of antidepressants have been reported in some studies, but the mechanisms underlying these effects remain unknown. Amitriptyline, a tricyclic antidepressant, is widely used in the management of psychological disorders and various types of pain, including neuropathic pain or fibromyalgia. In our previous work, we found the role of supraspinal mechanisms in the anti-inflammatory effect of amitriptyline. In the line of the indicated study, we sought to evaluate the effects of intraperitoneal (i.p.) and intracerebroventricular (i.c.v.) application of amitriptyline in the Carrageenan-Induced Paw Edema in rats in more details. Our findings confirmed that i.p. (40 and 80 mg/kg) and i.c.v. (100 μg/rat) injection of amitriptyline inhibited Carrageenan-Induced inflammation at different times. We also found that both i.p. and i.c.v. amitriptyline significantly decreased migration of polymorphonuclear (PMN) leucocytes into the site of inflammation, according to pathological evidence and the activity of myeloperoxidase (MPO). Furthermore, i.p. amitriptyline at the applied doses markedly reduced interleukin (IL)-1β and tumor necrosis factor (TNF)-α levels in the Paw treated with carrageenan. Our results also showed that i.c.v. amitriptyline noticeably decreased the concentration of IL-1β in the inflamed Paws. The TNF-α levels reduced in the i.c.v. group, even though these reductions were not statistically significant. These results confirmed the anti-inflammatory effects of systemic and central amitriptyline in the Carrageenan-Induced Paw Edema in rats, and demonstrated that these effects mediated mostly through the inhibition of PMN cells migration and release of IL-1β and TNF-α into the site of inflammation.