phenanthrenes and Neuralgia

phenanthrenes has been researched along with Neuralgia* in 4 studies

Other Studies

4 other study(ies) available for phenanthrenes and Neuralgia

ArticleYear
Antinociceptive and anti-inflammatory effects of cryptotanshinone through PI3K/Akt signaling pathway in a rat model of neuropathic pain.
    Chemico-biological interactions, 2019, May-25, Volume: 305

    Peripheral nerve injuries often induce neuropathic pain through inflammation. Cryptotanshinone isolated from Salvia miltiorrhiza Bunge has been found to exert anti-inflammatory and analgesic activities. Thus, this study aimed to determine whether cryptotanshinone inhibits chronic constriction injury (CCI)-induced neuropathic pain in rats and its mechanism of action. CCI was performed by applying four loose ligatures to rat sciatic nerve. Cryptotanshinone was orally administered using pre-surgery, acute or repeated post-surgery treatment. The pain behaviors were determined by recording paw withdrawal mechanical threshold (PWMT) and thermal withdrawal latency (TWL). ELISA kits were used to measure interleukin (IL)-6, IL-1β and tumor necrosis factor (TNF)-α levels. qRT-PCR were performed to detect IL-6, IL-1β, TNF-α, PI3K and Akt expression. The phosphorylation of PI3K/Akt signaling was assessed using western blotting. PWMT and TWL in CCI group were higher than those in the control and sham groups. The acute post-CCI cryptotanshinone treatment but not pre-surgery treatment reduced PWMT and TWL. The effect of cryptotanshinone is more prominent when it was repeatedly administered after CCI. The CCI-induced increase in IL-6, IL-1β, TNF-α, PI3K/Akt signaling and their phosphorylation was also suppressed by repeated post-CCI cryptotanshinone treatment. This study suggested that post-CCI cryptotanshinone treatment reduced the surgery-induced neuropathic pain by suppressing PI3K/Akt signaling therefore inhibited inflammation.

    Topics: Analgesics; Animals; Anti-Inflammatory Agents; Disease Models, Animal; Interleukin-1beta; Interleukin-6; Male; Neuralgia; Phenanthrenes; Phosphatidylinositol 3-Kinases; Phosphorylation; Proto-Oncogene Proteins c-akt; Rats; Rats, Sprague-Dawley; Salvia miltiorrhiza; Signal Transduction; Spinal Cord Dorsal Horn; Tumor Necrosis Factor-alpha

2019
Piperazine-2,3-dicarboxylic acid derivatives as dual antagonists of NMDA and GluK1-containing kainate receptors.
    Journal of medicinal chemistry, 2012, Jan-12, Volume: 55, Issue:1

    Competitive N-methyl-d-aspartate receptor (NMDAR) antagonists bind to the GluN2 subunit, of which there are four types (GluN2A-D). We report that some N(1)-substituted derivatives of cis-piperazine-2,3-dicarboxylic acid display improved relative affinity for GluN2C and GluN2D versus GluN2A and GluN2B. These derivatives also display subtype selectivity among the more distantly related kainate receptor family. Compounds 18i and (-)-4 were the most potent kainate receptor antagonists, and 18i was selective for GluK1 versus GluK2, GluK3 and AMPA receptors. Modeling studies revealed structural features required for activity at GluK1 subunits and suggested that S674 was vital for antagonist activity. Consistent with this hypothesis, replacing the equivalent residue in GluK3 (alanine) with a serine imparts 18i antagonist activity. Antagonists with dual GluN2D and GluK1 antagonist activity may have beneficial effects in various neurological disorders. Consistent with this idea, antagonist 18i (30 mg/kg ip) showed antinociceptive effects in an animal model of mild nerve injury.

    Topics: Analgesics; Animals; Binding Sites; Excitatory Postsynaptic Potentials; Female; HEK293 Cells; Hippocampus; Humans; In Vitro Techniques; Male; Models, Molecular; Neuralgia; Oocytes; Patch-Clamp Techniques; Peripheral Nerve Injuries; Phenanthrenes; Piperazines; Point Mutation; Protein Subunits; Rats; Rats, Wistar; Receptors, Kainic Acid; Receptors, N-Methyl-D-Aspartate; Recombinant Proteins; Stereoisomerism; Structure-Activity Relationship; Xenopus

2012
Intrathecal administration of triptolide, a T lymphocyte inhibitor, attenuates chronic constriction injury-induced neuropathic pain in rats.
    Brain research, 2012, Feb-03, Volume: 1436

    Triptolide is a potent immunosuppressive drug capable of inhibiting T cell activation and proliferation. Recent studies show that T cells play an important role in neuropathic pain following nerve injury in rats. In this study, we investigated the effect of triptolide on T cell activation and development of neuropathic pain. Neuropathic pain by chronic constriction injury (CCI) was induced by loose ligation of the sciatic nerve in Sprague-Dawley rats. Triptolide (5 or 10 μg/kg) or vehicle (DMSO) was administered intrathecally after surgery for 7 days (n=8 per group). The right hind paw withdrawal threshold to von Frey filament stimuli and withdrawal latency to radiant heat were determined before and after the surgery (days 0 to 7). NF-κB activation and pro-inflammatory cytokine (TNF-α and IL-2) expression were determined by ELISA, Western blot, and real time-PCR. CCI of the sciatic nerve induced mechanical allodynia and thermal hyperalgesia in these rats. Intrathecal triptolide (5 and 10 μg/kg) suppressed the development of allodynia and thermal hyperalgesia. It also inhibited CCI-induced inflammation and T cell activation, by decreasing spinal cord TNF-α, IL-2 and NF-κB p65 levels. Motor dysfunction was not observed after triptolide treatment. In the present study, we demonstrated the suppressive effect of triptolide on the development of neuropathic pain. Therefore, triptolide could be a promising immunosuppressive agent in the treatment of neuropathic pain. Further studies are required to examine the safety of intrathecal triptolide for clinical application.

    Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Chronic Pain; Diterpenes; Epoxy Compounds; Hyperalgesia; Interleukin-2; Lymphocyte Activation; Neuralgia; Phenanthrenes; Rats; Spinal Cord Injuries; T-Lymphocytes; Transcription Factor RelA; Tumor Necrosis Factor-alpha

2012
Spinal cannabinoid receptor type 2 agonist reduces mechanical allodynia and induces mitogen-activated protein kinase phosphatases in a rat model of neuropathic pain.
    The journal of pain, 2012, Volume: 13, Issue:9

    Peripheral nerve injury generally results in spinal neuronal and glial plastic changes associated with chronic behavioral hypersensitivity. Spinal mitogen-activated protein kinases (MAPKs), eg, p38 or extracellular signal-regulated kinases (ERKs), are instrumental in the development of chronic allodynia in rodents, and new p38 inhibitors have shown potential in acute and neuropathic pain patients. We have previously shown that the cannabinoid type 2 receptor agonist JWH015 inhibits ERK activity by inducing MAPK phosphatase (MKP)-1 and MKP-3 (the major regulators of MAPKs) in vitro in microglial cells. Therefore, we decided to investigate the role of these phosphatases in the mechanisms of action of JWH015 in vivo using the rat L5 nerve transection model of neuropathic pain. We observed that peripheral nerve injury reduced spinal MKP-1/3 expression and activity and that intrathecal JWH015 reduced established L5 nerve injury-induced allodynia, enhanced spinal MKP-1/3 expression and activity, and reduced the phosphorylated form of p38 and ERK-1/2. Triptolide, a pharmacological blocker of MKP-1 and MKP-3 expression, inhibited JWH015's effects, suggesting that JWH015 exerts its antinociceptive effects by modulating MKP-1 and MKP-3. JWH015-induced antinociception and MKP-1 and MKP-3 expression were inhibited by the cannabinoid type 2 receptor antagonist AM630. Our data suggest that MKP-1 and MKP-3 are potential targets for novel analgesic drugs.. MAPKs are pivotal in the development of chronic allodynia in rodent models of neuropathic pain. A cannabinoid type 2 receptor agonist, JWH015, reduced neuropathic allodynia in rats by reducing MAPK phosphorylation and inducing spinal MAPK phosphatases 1 and 3, the major regulators of MAPKs.

    Topics: 4-Nitrophenylphosphatase; Animals; Disease Models, Animal; Diterpenes; Dual Specificity Phosphatase 1; Dual Specificity Phosphatase 6; Epoxy Compounds; Gene Expression Regulation; Hyperalgesia; Immunosuppressive Agents; Indoles; Male; Mitogen-Activated Protein Kinase Phosphatases; Nerve Tissue Proteins; Neuralgia; Phenanthrenes; Rats; Rats, Sprague-Dawley; Receptor, Cannabinoid, CB2; Signal Transduction; Spinal Cord; Time Factors

2012