scholarly journals Plant Derived Aporphinic Alkaloid S-(+)-Dicentrine Induces Antinociceptive Effect in Both Acute and Chronic Inflammatory Pain Models: Evidence for a Role of TRPA1 Channels

PLoS ONE ◽  
2013 ◽  
Vol 8 (7) ◽  
pp. e67730 ◽  
Author(s):  
Deise Prehs Montrucchio ◽  
Marina Machado Córdova ◽  
Adair Roberto Soares Santos
Keyword(s):  
Inflammatory Pain ◽  
Antinociceptive Effect ◽  
Chronic Inflammatory Pain ◽  
Pain Models

scholarly journals Is Hippocampus Susceptible to Antinociceptive Tolerance to NSAIDs Like the Periaqueductal Grey?

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Nana Tsiklauri ◽  
Ivliane Nozadze ◽  
Gulnazi Gurtskaia ◽  
Merab G. Tsagareli
Keyword(s):  
Dorsal Hippocampus ◽  
Antinociceptive Effect ◽  
Male Rats ◽  
Opioid Antagonist ◽  
Tail Flick ◽  
Pain Models ◽  
Inflammatory Drugs ◽  
Antinociceptive Tolerance ◽  
Undesirable Feature

Emotional distress is the most undesirable feature of painful experience. Numerous studies have demonstrated the important role of the limbic system in the affective-motivational component of pain. The purpose of this paper was to examine whether microinjection of nonsteroidal anti-inflammatory drugs (NSAIDs), Clodifen, Ketorolac, and Xefocam, into the dorsal hippocampus (DH) leads to the development of antinociceptive tolerance in male rats. We found that microinjection of these NSAIDs into the DH induces antinociception as revealed by a latency increase in the tail-flick (TF) and hot plate (HP) tests compared to controls treated with saline into the DH. Subsequent tests on consecutive three days, however, showed that the antinociceptive effect of NSAIDs progressively decreased, suggesting tolerance developed to this effect of NSAIDs. Both pretreatment and posttreatment with the opioid antagonist naloxone into the DH significantly reduced the antinociceptive effect of NSAIDs in both pain models. Our data indicate that microinjection of NSAIDs into the DH induces antinociception which is mediated via the opioid system and exhibits tolerance.

scholarly journals Blockade of Adrenal Medulla-Derived Epinephrine Potentiates Bee Venom-Induced Antinociception in the Mouse Formalin Test: Involvement of Peripheralβ-Adrenoceptors

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Suk-Yun Kang ◽  
Dae-Hyun Roh ◽  
Hyun-Woo Kim ◽  
Ho-Jae Han ◽  
Alvin J. Beitz ◽  
...  
Keyword(s):  
Adrenal Medulla ◽  
Formalin Test ◽  
Late Phase ◽  
Antinociceptive Effect ◽  
Bee Venom ◽  
Pain Models ◽  
Adrenergic Antagonists ◽  
Novel Strategy ◽  
Chronic Pain Conditions

The injection of diluted bee venom (DBV) into an acupoint has been used traditionally in eastern medicine to treat a variety of inflammatory chronic pain conditions. We have previously shown that DBV had a potent antinociceptive efficacy in several rodent pain models. However, the peripheral mechanisms underlying DBV-induced antinociception remain unclear. The present study was designed to investigate the role of peripheral epinephrine on the DBV-induced antinociceptive effect in the mouse formalin assay. Adrenalectomy significantly enhanced the antinociceptive effect of DBV during the late phase of the formalin test, while chemical sympathectomy had no effect. Intraperitoneal injection of epinephrine blocked this adrenalectomy-induced enhancement of the DBV-induced antinociceptive effect. Moreover, injection of a phenylethanolamine N-methyltransferase (PNMT) inhibitor enhanced the DBV-induced antinociceptive effect. Administration of nonselectiveβ-adrenergic antagonists also significantly potentiated this DBV-induced antinociception, in a manner similar to adrenalectomy. These results demonstrate that the antinociceptive effect of DBV treatment can be significantly enhanced by modulation of adrenal medulla-derived epinephrine and this effect is mediated by peripheralβ-adrenoceptors. Thus, DBV acupoint stimulation in combination with inhibition of peripheralβ-adrenoceptors could be a potentially novel strategy for the management of inflammatory pain.

scholarly journals The antinociceptive effect of artemisinin on the inflammatory pain and role of GABAergic and opioidergic systems

2019 ◽  
Vol 32 (3) ◽  
pp. 160-167 ◽  
Author(s):  
Faraz Mahdian Dehkordi ◽  
Jahangir Kaboutari ◽  
Morteza Zendehdel ◽  
Moosa Javdani
Keyword(s):  
Inflammatory Pain ◽  
Antinociceptive Effect

scholarly journals Anti-hyperalgesic properties of a flavanone derivative Poncirin in acute and chronic inflammatory pain models in mice

2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Ruqayya Afridi ◽  
Ashraf Ullah Khan ◽  
Sidra Khalid ◽  
Bushra Shal ◽  
Hina Rasheed ◽  
...  
Keyword(s):  
Acetic Acid ◽  
Mrna Expression ◽  
Inflammatory Cytokines ◽  
Inflammatory Pain ◽  
Expression Levels ◽  
Chronic Inflammatory Pain ◽  
Qrt Pcr ◽  
Pain Models ◽  
Anti Oxidant ◽  
Mrna Expression Levels

Abstract Background Poncirin is flavanone derivative (isolated from Poncirus trifoliata) with known pharmacological activities such as anti-tumor, anti-osteoporotic, anti-inflammatory and anti-colitic. The present study aimed to explore the anti-allodynic and anti-hyperalgesic potentials of poncirin in murine models of inflammatory pain. Methods The analgesic potential of poncirin was evaluated in formalin-, acetic acid-, carrageenan- and Complete Freund’s Adjuvant (CFA)-induced inflammatory pain models in mice. Anti-allodynic and anti-hyperalgesic activities were measured using Von Frey filaments, Randall Selitto, hotplate and cold acetone tests. The serum nitrite levels were determined using Griess reagent. The Quantitative Real-time PCR (qRT-PCR) was performed to assess the effect of poncirin on mRNA expression levels of inflammatory cytokines and anti-oxidant enzymes. Results Intraperitoneal administration of poncirin (30 mg/kg) markedly reduced the pain behavior in both acetic acid-induced visceral pain and formalin-induced tonic pain models used as preliminary screening tools. The poncirin (30 mg/kg) treatment considerably inhibited the mechanical hyperalgesia and allodynia as well as thermal hyperalgesia and cold allodynia. The qRT-PCR analysis showed noticeable inhibition of pro-inflammatory cytokines (mRNA expression levels of TNF-α, IL-1β and IL-6) (p < 0.05) in poncirin treated group. Similarly, poncirin treatment also enhanced the mRNA expressions levels of anti-oxidant enzymes such as transcription factor such as nuclear factor (erythroid-derived 2)-like 2 (Nrf2) (p < 0.05), heme oxygenase (HO-1) (p < 0.05) and superoxide dismutase (SOD2) (p < 0.05). Chronic treatment of poncirin for 6 days did not confer any significant hepatic and renal toxicity. Furthermore, poncirin treatment did not altered the motor coordination and muscle strength in CFA-induced chronic inflammatory pain model. Conclusion The present study demonstrated that poncirin treatment significantly reduced pain behaviors in all experimental models of inflammatory pain, suggesting the promising analgesic potential of poncirin in inflammatory pain conditions.

scholarly journals Neutrophilic Cell-Free Exudate Induces Antinociception Mediate by the Protein S100A9

2006 ◽  
Vol 2006 ◽  
pp. 1-6 ◽  
Author(s):  
Rosana L. Pagano ◽  
Mario Mariano ◽  
Renata Giorgi
Keyword(s):  
Monoclonal Antibody ◽  
Calcium Binding ◽  
Inflammatory Pain ◽  
Initial Phase ◽  
Binding Protein ◽  
Antinociceptive Effect ◽  
Calcium Binding Protein ◽  
Nociceptive Response ◽  
Endogenous Control

Calcium-binding protein S100A9 (MRP-14) induces antinociceptive effect in an experimental model of painful sensibility and participates of antinociception observed during neutrophilic peritonitis induced by glycogen or carrageenan in mice. In this study, the direct antinociceptive role of the protein S100A9 in neutrophilic cell-free exudates obtained of mice injected with glycogen was investigated. Mice were intraperitoneally injected with a glycogen solution, and after4,8,24, and48hours, either the pattern of cell migration of the peritoneal exudate or the nociceptive response of animals was evaluated. The glycogen-induced neutrophilic peritonitis evoked antinociception4and8hours after inoculation of the irritant. Peritoneal cell-free exudates, collected in different times after the irritant injection, were transferred to naive animals which were submitted to the nociceptive test. The transference of exudates also induced antinociceptive effect, and neutralization of S100A9 activity by anti-S100A9 monoclonal antibody totally reverted this response. This effect was not observed when experiments were made24or48hours after glycogen injection. These results clearly indicate that S100A9 is secreted during glycogen-induced neutrophilic peritonitis, and that this protein is responsible by antinociception observed in the initial phase of inflammatory reaction. Thus, these data reinforce the hypothesis that the calcium-binding protein S100A9 participates of the endogenous control of inflammatory pain.

Antinociceptive Properties of Protein C in a Model of Inflammatory Hyperalgesia in Rats

1995 ◽  
Vol 73 (02) ◽  
pp. 252-255 ◽  
Author(s):  
L Pichler ◽  
W Schramm ◽  
W Ulrich ◽  
K Varadi ◽  
H P Schwarz
Keyword(s):  
Inflammatory Pain ◽  
Protein C ◽  
Pain Threshold ◽  
Antinociceptive Effect ◽  
Pretreatment Level ◽  
Intraplantar Injection ◽  
Inflammatory Hyperalgesia ◽  
The Mean ◽  
Dose Dependent

SummaryWe investigated the role of human protein C in an animal model of inflammatory hyperalgesia. Pain was induced by intraplantar injection of carrageenan (3 mg) into the hind paw of rats. The pain threshold was measured by exerting increasing amounts of pressure (in mmHg) on the paw until a struggle reaction was observed. Protein C (8-800 IU/kg) was administered intravenously immediately after carrageenan. Controls received either intraplantar injections of saline (100 µ1) instead of carrageenan or carrageenan alone. Effects on pain threshold were expressed in percent of the pretreatment value. Carrageenan alone lowered the mean pain threshold after 3 h to 33.2 ± 2.2% of the pretreatment level. Addition of protein C resulted in a dose-dependent rise in pain threshold towards the level observed in control animals treated with saline instead of carrageenan (pain threshold after 800 IU/kg protein C = 62.9 ± 2.3% of pretreatment level), demonstrating an antinociceptive effect. Protein C had no effect in animals not preconditioned with intraplantar carrageenan. Thus protein C clearly antagonized the inflammatory pain induced by carrageenan. The antinociceptive action of protein C was antagonized by injection of a monoclonal antibody against protein C, providing additional evidence that the effect was protein C-mediated.

scholarly journals Role of NGF in Neuronal Plasticity in the Lateral Reticular Nucleus in Chronic Inflammatory Pain

2009 ◽  
Vol 2 (1) ◽  
pp. 41-52 ◽  
Author(s):  
Sophie Pezet ◽  
Fabien Marchand ◽  
Karine Thibault ◽  
Celine Dauvergne ◽  
John Grist ◽  
...  
Keyword(s):  
Neuronal Plasticity ◽  
Inflammatory Pain ◽  
Reticular Nucleus ◽  
Lateral Reticular Nucleus ◽  
Chronic Inflammatory Pain

scholarly journals Cav3.2 calcium channels involvement in inflammation and related pain-like symptoms in murine inflammatory models

2021 ◽  
Author(s):  
Elodie Picard ◽  
Nicolas Kerckhove ◽  
Amaury François ◽  
Ludivine Boudieu ◽  
Elisabeth Billard ◽  
...  
Keyword(s):  
Calcium Channels ◽  
Inflammatory Pain ◽  
Fluorescent Protein ◽  
Pharmacological Agents ◽  
Inflammatory Models ◽  
Pain Models ◽  
Low Threshold ◽  
Green Fluorescent ◽  
First Time

Background and Purpose T-type calcium channels, mainly the Cav3.2 subtype, are important contributors to the nociceptive signaling pathway. We investigated their involvement in inflammation and related pain-like symptoms. Experimental Approach The involvement of Cav3.2 and T-type channels was investigated using genetic and pharmacological inhibition to assess mechanical allodynia/hyperalgesia and edema development in two murine inflammatory pain models. The location of Cav3.2 involved in pain-like symptoms was studied in mice with Cav3.2 knocked out in C-low threshold mechanoreceptors (C-LTMR) and the use of ABT-639, a peripherally restricted T-type channel inhibitor. The anti-edematous effect of Cav3.2 inhibition was investigated in chimeric mice with immune cells deleted for Cav3.2. Lymphocytes and macrophages from either green fluorescent protein-targeted Cav3.2 or KO mice were used to determine the expression of Cav3.2 protein and the functional status of the cells. Key Results We showed the role of Cav3.2 channels in the development of pain-like symptoms and edema in the two murine inflammatory pain models. For the first time, we provide evidence of the involvement of Cav3.2 channels located on C-LTMRs in inflammatory pain at both peripheral and primary afferent terminals at the spinal level. We showed that Cav3.2 channels located in T cells and macrophages contribute to the inflammatory process. Conclusion and Implications This work highlights the crucial role of Cav3.2 channels in inflammation and related pain and suggests that targeting Cav3.2 channels with pharmacological agents could be an attractive and readily evaluable strategy in a clinical trial to relieve chronic inflammatory pain in affected patients.

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