strychnine has been researched along with Inflammation* in 13 studies
13 other study(ies) available for strychnine and Inflammation
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Pharmacognostic profiles, evaluation of analgesic, anti-inflammatory and anticonvulsant activities of Newbouldia laevis (P. Beauv.) Seem. ex Bureau leaf and root extracts in Wistar rats.
Newbouldia laevis is a popular medicinal plant whose leaves and roots are used in Nigeria as ethnomedicinal prescriptions for pain, inflammation, convulsion, and epilepsy. These claims have not been scientifically verified prior to this study.. To determine pharmacognostic profiles of the leaves and roots and evaluate the analgesic, anti-inflammatory, and anticonvulsant activities of methanol leaf and root extracts in Wistar rats.. The pharmacognostic profiles of the leaves and roots were determined using standard procedures to serve as fingerprints for the plant. The methanol leaf and root extracts of Newbouldia laevis were tested for acute toxicity using the OECD's up and down method at the maximum dose of 2000 mg/kg (orally) in Wistar rats. Analgesic studies were carried out in acetic acid-induced writhing in rats and tail immersion. The anti-inflammatory activity of the extracts was evaluated using carrageenan-induced rat paw-oedema and formalin-induced inflammation in rats' mode. The anticonvulsant activity was determined using strychnine-induced, pentylenetetrazol-induced, and maximal electroshock-induced rat convulsion models. For each of these studies, the extracts doses of 100, 200 and 400 mg/kg were administered to the rats following the oral route.. Our study revealed some pharmacognostic profiles of Newbouldia laevis leaves and roots that are vital for its identification from closely related species often used for adulteration in traditional medicine. The study further showed that the leaf and root extracts of the plant possessed dose-dependent analgesics, anti-inflammatory and anti-convulsant activities in rats, thus, justifying its use for the treatment of these diseases in Nigerian traditional medicine. There is a need to further study its mechanisms of action towards drug discovery. Topics: Analgesics; Animals; Anti-Inflammatory Agents; Anticonvulsants; Edema; Inflammation; Methanol; Pentylenetetrazole; Plant Extracts; Plant Leaves; Rats; Rats, Wistar; Seizures; Strychnine | 2023 |
Brucine promotes apoptosis in cervical cancer cells (ME-180) via suppression of inflammation and cell proliferation by regulating PI3K/AKT/mTOR signaling pathway.
Brucine are the main constituents of Strychnos nux-vomica. Earlier reports have determined brucine shows anti-inflammatory, analgesic and excellent anti-tumor drug. Even though its anticervical cancer cells remains not clearly evaluated. So that, we hypothesized the anti-cervical cancer activity of brucine against the cervical (ME-180) cells. Brucine inhibited the inflammation, cell proliferation and promoted rate of apoptotic cell death ad reduced the mitochondrial potential, which is evidenced by respective (AO/EB, Rh-123, and PI) staining. Furthermore ELISA and real time PCR reaction determined that brucine were down regulated inflammatory (TNF-α, NF-kB, IL-6 & COX-2) cell proliferation (Cyclin D1) and apoptotic marker Bax, caspase-3, PI3K (phosphoinosital 3 kinase), AKT, mTOR (mammalian target of rapamycin) and over expression Bcl-2, associated death promoter. These findings were confirmed and finally suggested that brucine inhibited inflammation, cell proliferation and promoted the apoptosis through the down-regulation of PI3K/AKT/mTOR pathway. Taken together, these data were exhibited brucine as a good therapeutic agents for the prevention of anticancer cervical cancer drugs. Topics: Apoptosis; Cell Line, Tumor; Cell Proliferation; Female; Humans; Inflammation; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; Signal Transduction; Strychnine; TOR Serine-Threonine Kinases; Uterine Cervical Neoplasms | 2021 |
Involvement of glycine receptor α1 subunits in cannabinoid-induced analgesia.
Some cannabinoids have been shown to suppress chronic pain by targeting glycine receptors (GlyRs). Although cannabinoid potentiation of α3 GlyRs is thought to contribute to cannabinoid-induced analgesia, the role of cannabinoid potentiation of α1 GlyRs in cannabinoid suppression of chronic pain remains unclear. Here we report that dehydroxylcannabidiol (DH-CBD), a nonpsychoactive cannabinoid, significantly suppresses chronic inflammatory pain caused by noxious heat stimulation. This effect may involve spinal α1 GlyRs since the expression level of α1 subunits in the spinal cord is positively correlated with CFA-induced inflammatory pain and the GlyRs antagonist strychnine blocks the DH-CBD-induced analgesia. A point-mutation of S296A in TM3 of α1 GlyRs significantly inhibits DH-CBD potentiation of glycine currents (I Topics: Action Potentials; Analgesics; Animals; Animals, Genetically Modified; Cannabinoids; Cyclohexanones; Disease Models, Animal; Dose-Response Relationship, Drug; Female; Freund's Adjuvant; Gene Expression Regulation; Glycine Agents; HEK293 Cells; Humans; In Vitro Techniques; Inflammation; Male; Mice; Mice, Inbred C57BL; Mutation; Neurons; Pain; Pain Measurement; Patch-Clamp Techniques; Receptors, Glycine; Reflex, Startle; Rotarod Performance Test; Spinal Cord; Strychnine; Time Factors; Transfection | 2018 |
Antinociceptive effect of intracerebroventricular administration of glycine transporter-2 inhibitor ALX1393 in rat models of inflammatory and neuropathic pain.
Glycinergic transmission has an important role in regulating nociception in the spinal cord. The glycine transporter-2 (GlyT2) is localized at presynaptic terminals of glycinergic neurons and eliminates glycine from the synaptic cleft to terminate glycinergic transmission. Systemic and intrathecal administration of GlyT2 inhibitors alleviate various types of pain. Although the GlyT2s and glycine receptors are widely distributed in the central nervous system, little is known about the role of glycinergic transmission in pain perception at supraspinal regions. The present study examined the antinociceptive effect of intracerebroventricular (i.c.v.) administration of the selective GlyT2 inhibitor ALX1393 on inflammatory and neuropathic pain in experimental models. For i.c.v. administration, a guide cannula was implanted into the right lateral ventricle of male Sprague-Dawley rats. Normal rats were used to assess inflammatory nociception using the formalin test and motor function using the rotarod test. Chronic constriction injury (CCI) to the sciatic nerve was induced in the rats. The CCI rats were then used to assess mechanical, cold, and thermal hyperalgesia using the electronic von Frey test, cold plate test, and the plantar test, respectively. ALX1393 (25, 50, and 100 μg) was administered i.c.v. to examine its effects on supraspinal antinociception. Supraspinal ALX1393 in normal rats suppressed the late-phase response in the formalin test but did not affect motor performance. In the CCI rats, ALX1393 inhibited mechanical and cold hyperalgesia in a dose-dependent manner. The antihyperalgesic effects of ALX1393 (100 μg) were reversed completely by i.c.v. pretreatment with a glycine receptor antagonist strychnine (10 μg). These results suggest that GlyT2 contributes to nociceptive transmission at supraspinal level and that the selective GlyT2 inhibitor is a promising candidate for the treatment of inflammatory and neuropathic pain without causing motor dysfunction. Topics: Analgesics; Animals; Disease Models, Animal; Dose-Response Relationship, Drug; Glycine Plasma Membrane Transport Proteins; Hyperalgesia; Inflammation; Infusions, Intraventricular; Male; Neuralgia; Pain; Pain Measurement; Rats; Rotarod Performance Test; Serine; Strychnine | 2015 |
Inflammatory Pain Promotes Increased Opioid Self-Administration: Role of Dysregulated Ventral Tegmental Area μ Opioid Receptors.
Pain management in opioid abusers engenders ethical and practical difficulties for clinicians, often resulting in pain mismanagement. Although chronic opioid administration may alter pain states, the presence of pain itself may alter the propensity to self-administer opioids, and previous history of drug abuse comorbid with chronic pain promotes higher rates of opioid misuse. Here, we tested the hypothesis that inflammatory pain leads to increased heroin self-administration resulting from altered mu opioid receptor (MOR) regulation of mesolimbic dopamine (DA) transmission. To this end, the complete Freund's adjuvant (CFA) model of inflammation was used to assess the neurochemical and functional changes induced by inflammatory pain on MOR-mediated mesolimbic DA transmission and on rat intravenous heroin self-administration under fixed ratio (FR) and progressive ratio (PR) schedules of reinforcement. In the presence of inflammatory pain, heroin intake under an FR schedule was increased for high, but attenuated for low, heroin doses with concomitant alterations in mesolimbic MOR function suggested by DA microdialysis. Consistent with the reduction in low dose FR heroin self-administration, inflammatory pain reduced motivation for a low dose of heroin, as measured by responding under a PR schedule of reinforcement, an effect dissociable from high heroin dose PR responding. Together, these results identify a connection between inflammatory pain and loss of MOR function in the mesolimbic dopaminergic pathway that increases intake of high doses of heroin. These findings suggest that pain-induced loss of MOR function in the mesolimbic pathway may promote opioid dose escalation and contribute to opioid abuse-associated phenotypes.. This study provides critical new insights that show that inflammatory pain alters heroin intake through a desensitization of MORs located within the VTA. These findings expand our knowledge of the interactions between inflammatory pain and opioid abuse liability, and should help to facilitate the development of novel and safer opioid-based strategies for treating chronic pain. Topics: Action Potentials; Analgesics, Opioid; Animals; Conditioning, Operant; Disease Models, Animal; Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; Excitatory Amino Acid Antagonists; Glycine Agents; Heroin; Hyperalgesia; Inflammation; Inhibitory Postsynaptic Potentials; Male; Neurons; Pain; Pain Threshold; Quinoxalines; Rats; Rats, Sprague-Dawley; Receptors, Opioid, mu; Strychnine; Sucrose; Ventral Tegmental Area | 2015 |
Strychnine inhibits inflammatory angiogenesis in mice via down regulation of VEGF, TNF-α and TGF-β.
Strychnine is known to possess anti-inflammatory and antitumour activity, but its roles in tumour angiogenesis, the key step involved in tumour growth and metastasis, and the involved molecular mechanism are still unknown. We aimed to investigate the effects of strychnine on key components of inflammatory angiogenesis in the murine cannulated sponge implant angiogenesis model. Polyester-polyurethane sponges, used as a framework for fibrovascular tissue growth, were implanted in Swiss albino mice and strychnine (0.25, and 0.5 mg/kg/day) was given through installed cannulas for 9 days. The implants collected at day 9 postimplantation were processed for the assessment of haemoglobin (Hb), myeloperoxidase (MPO), N-acetylglucosaminidase (NAG) and collagen used as indexes for angiogenesis, neutrophil and macrophage accumulation and extracellular matrix deposition, respectively. Relevant inflammatory, angiogenic and fibrogenic cytokines were also determined. Strychnine treatment attenuated the main components of the fibrovascular tissue, wet weight, vascularization (Hb content), macrophage recruitment (NAG activity), collagen deposition and the levels of vascular endothelial growth factor (VEGF), tumour necrosis factor (TNF)-α and transforming growth factor (TGF-β). A regulatory function of strychnine on multiple parameters of main components of inflammatory angiogenesis has been revealed giving insight into the potential therapeutic underlying the actions of strychnine. Topics: Acetylglucosaminidase; Angiogenesis Inhibitors; Animals; Anti-Inflammatory Agents; Biomarkers; Collagen; Dose-Response Relationship, Drug; Down-Regulation; Extracellular Matrix; Hemoglobins; Inflammation; Inflammation Mediators; Macrophages; Male; Mice; Neovascularization, Pathologic; Neutrophils; Peroxidase; Polyesters; Polyurethanes; Strychnine; Surgical Sponges; Time Factors; Transforming Growth Factor beta; Tumor Necrosis Factor-alpha; Vascular Endothelial Growth Factor A | 2013 |
[Brucine chitosan thermosensitive hydrogel for intra-articular injection].
The aim of this study was to develop a sustained release converse thermosensitive hydrogel for intra-articular injection using chitosan-glycerol-borax as matrix, its physical properties and biocompatibility were investigated. Taking gelation time and gelation condition as index, the influence of concentration of chitosan, ratio of chitosan to glycerol, pH on physical properties of hydrogel were investigated. And then the in vitro drug release, rheological properties and biocompatibility were studied. The thermosensitive hydrogel flows easily at room temperature and turns to gelation at body temperature, which can certainly prolong the release of drug and has good biocompatibility. Topics: Analgesics; Animals; Chitosan; Delayed-Action Preparations; Drug Compounding; Hydrogels; Hydrogen-Ion Concentration; Inflammation; Injections, Intra-Articular; Knee Joint; Male; Materials Testing; Plants, Medicinal; Rats; Rats, Sprague-Dawley; Rheology; Seeds; Strychnine; Strychnos nux-vomica; Surface Properties; Synaptic Membranes; Temperature | 2012 |
The inhibitory neurotransmitter glycine modulates macrophage activity by activation of neutral amino acid transporters.
Glycine, an important inhibitory neurotransmitter in the mammalian central nervous system (CNS), has been shown to modulate peripheral immune cell responses. In that respect, glycine levels are increased in several neuroinflammatory disorders, such as amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS). In this study, we show that glycine modulates macrophage effector functions implicated in CNS inflammation and in other, related inflammatory conditions. We demonstrate that glycine does not affect the production of reactive oxygen species but stimulates myelin phagocytosis and the production of the proinflammatory mediators nitric oxide (NO) and tumor necrosis factor (TNF)-alpha by rat macrophages. These effects of glycine are not mediated by the glycine receptor (GlyR) or by glycine transporters (GlyTs), as neither the GlyR antagonist strychnine nor the antagonist of GlyT1 (ALX5407) reverses the observed effects. In contrast, 2-aminoisobutyric acid, a substrate of neutral amino acid transporters (NAATs), inhibits the glycine-mediated enhancement of myelin phagocytosis as well as of NO and TNF-alpha production. In conclusion, our findings demonstrate that glycine modulates macrophage function through activation of NAATs. Glycine may thereby influence immunological processes in inflammatory diseases involving macrophage activation and demyelination, including MS and related conditions associated with altered glycine levels. Topics: Amino Acid Transport Systems, Neutral; Animals; Biotransformation; Cell Proliferation; Cell Survival; Dose-Response Relationship, Drug; Fluorescent Antibody Technique; Glycine; Glycine Agents; Inflammation; Macrophages, Peritoneal; Male; Multiple Sclerosis; Myelin Sheath; Neurotransmitter Agents; Nitric Oxide; Phagocytosis; Rats; Rats, Wistar; Reactive Oxygen Species; Receptors, Glycine; Reverse Transcriptase Polymerase Chain Reaction; Strychnine; Tumor Necrosis Factor-alpha | 2010 |
Fast non-genomic effects of progesterone-derived neurosteroids on nociceptive thresholds and pain symptoms.
Fast Inhibitory controls mediated by glycine (GlyRs) and GABAA receptors (GABAARs) play an important role to prevent the apparition of pathological pain symptoms of allodynia and hyperalgesia. The use of positive allosteric modulators of these receptors, specifically expressed in the spinal cord, may represent an interesting strategy to limit or block pain expression. In this study, we have used stereoisomers of progesterone metabolites, acting only via non-genomic effects, in order to evaluate the contribution of GlyRs and GABAARs for the reduction of mechanical and thermal heat hypernociception. We show that 3alpha neurosteroids were particularly efficient to elevate nociceptive thresholds in naive animal. It also reduced mechanical allodynia and thermal heat hyperalgesia in the carrageenan model of inflammatory pain. This effect is likely to be mediated by GABAA receptors since 3beta isomer was inefficient. More interestingly, 3alpha5beta neurosteroid was only efficient on mechanical allodynia while having no effect on thermal heat hyperalgesia. We characterized these paradoxical effects of 3alpha5beta neurosteroid using the strychnine and bicuculline models of allodynia. We clearly show that 3alpha5beta neurosteroid exerts an antinociceptive effect via a positive allosteric modulation of GABAARs but, at the same time, is pronociceptive by reducing GlyR function. This illustrates the importance of the inhibitory amino acid receptor channels and their allosteric modulators in spinal pain processing. Moreover, our results indicate that neurosteroids, which are synthesized in the dorsal horn of the spinal cord and have limited side effects, may be of significant interest in order to treat pathological pain symptoms. Topics: Allosteric Regulation; Analgesics, Non-Narcotic; Animals; Bicuculline; Carrageenan; Drug Evaluation, Preclinical; Hot Temperature; Hyperalgesia; Inflammation; Male; Molecular Conformation; Pain Threshold; Pregnanolone; Rats; Rats, Sprague-Dawley; Receptors, GABA-A; Receptors, Glycine; Spinal Cord; Stereoisomerism; Structure-Activity Relationship; Strychnine; Touch | 2008 |
Reduction of glycine receptor-mediated miniature inhibitory postsynaptic currents in rat spinal lamina I neurons after peripheral inflammation.
Peripheral inflammation may induce long-lasting sensitization in the central nociceptive system. Neurons in lamina I of the spinal dorsal horn play a pivotal role in the integration and relay of pain-related information. In rats we studied whether changes in passive and active membrane properties and/or alteration of glycine receptor-mediated inhibitory control of spinal lamina I neurons may contribute to central sensitization in a model of peripheral long-lasting inflammation (complete Freund's adjuvant, hindpaw). Spontaneously occurring glycine receptor-mediated miniature inhibitory postsynaptic currents (GlyR-mediated mIPSCs) were recorded in lumbar spinal lamina I neurons. Miniature IPSC rise, decay kinetics and mean GlyR-mediated mIPSC amplitude were not affected by peripheral inflammation. The mean frequency of GlyR-mediated mIPSCs of lamina I neurons ipsilateral to the inflamed hindpaw was, however, significantly reduced by peripheral inflammation when compared with neurons from noninflamed animals. Principal passive and active membrane properties and firing patterns of spinal lamina I neurons were not changed by inflammation. These results indicate that long-lasting peripheral inflammation leads to a reduced glycinergic inhibitory control of spinal lamina I neurons by a presynaptic mechanism. Topics: 6-Cyano-7-nitroquinoxaline-2,3-dione; Anesthetics, Local; Animals; Animals, Newborn; Bicuculline; Drug Interactions; Excitatory Amino Acid Antagonists; Excitatory Postsynaptic Potentials; Female; Freund's Adjuvant; GABA Antagonists; Glycine Agents; In Vitro Techniques; Inflammation; Male; Membrane Potentials; Neural Inhibition; Neurons; Patch-Clamp Techniques; Rats; Rats, Sprague-Dawley; Receptors, Glycine; Spinal Cord; Strychnine; Synapses; Tetrodotoxin; Valine | 2003 |
Neural mechanisms of lameness.
Topics: Anesthesia; Animals; Brain Stem; Cats; Cerebral Cortex; Electric Stimulation; Electrophysiology; Hindlimb; Inflammation; Mesencephalon; Movement Disorders; Neurons; Pyramidal Tracts; Reflex; Reflex, Monosynaptic; Sciatic Nerve; Spinal Cord; Strychnine; Synapses; Thalamus | 1968 |
INHIBITORY SYNAPSES AND INFLAMMATION.
Topics: Brain; Cats; Cerebral Cortex; Electrophysiology; Inflammation; Injections, Intravenous; Motor Neurons; Neural Conduction; Nitrates; Reflex; Research; Strychnine; Synapses; Thalamus; Toxicology; Turpentine | 1965 |
[Significance of inhibitory synapses in the compensatory mechanism of disturbed functions].
Topics: Animals; Cerebral Cortex; Electrophysiology; Extremities; Inflammation; Neurons; Reflex; Spinal Nerves; Strychnine; Synapses | 1965 |