Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 4 de 4
Filter
Add more filters

Therapeutic Methods and Therapies TCIM
Database
Language
Affiliation country
Publication year range
2.
Mol Brain ; 12(1): 36, 2019 04 08.
Article in English | MEDLINE | ID: mdl-30961625

ABSTRACT

Chronic pain is commonly accompanied with anxiety disorder, which complicates treatment. In this study, we investigated the analgesic and anxiolytic effects of Formononetin (FMNT), an active component of traditional Chinese medicine red clover (Trifolium pratense L.) that is capable of protecting neurons from N-methyl-D-aspartate (NMDA)-evoked excitotoxic injury, on mice suffering from complete Freund's adjuvant (CFA)-induced chronic inflammatory pain. The results show that FMNT administration significantly reduces anxiety-like behavior but does not affect the nociceptive threshold in CFA-injected mice. The treatment reverses the upregulation of NMDA, GluA1, and GABAA receptors, as well as PSD95 and CREB in the basolateral amygdala (BLA). The effects of FMNT on NMDA receptors and CREB binding protein (CBP) were further confirmed by the potential structure combination between these compounds, which was analyzed by in silico docking technology. FMNT also inhibits the activation of the NF-κB signaling pathway and microglia in the BLA of mice suffering from chronic inflammatory pain. Therefore, the anxiolytic effects of FMNT are partially due to the attenuation of inflammation and neuronal hyperexcitability through the inhibition of NMDA receptor and CBP in the BLA.


Subject(s)
Anti-Anxiety Agents/therapeutic use , Anxiety/therapy , Inflammation/pathology , Isoflavones/therapeutic use , Animals , Anti-Anxiety Agents/pharmacology , Basolateral Nuclear Complex/metabolism , Behavior, Animal/drug effects , Cyclic AMP Response Element-Binding Protein/metabolism , Disease Models, Animal , Freund's Adjuvant , Isoflavones/chemistry , Isoflavones/pharmacology , Male , Mice, Inbred C57BL , Microglia/drug effects , Microglia/metabolism , Microglia/pathology , Models, Molecular , NF-kappa B/metabolism , NF-kappa B/pharmacokinetics , Pain/drug therapy , Receptors, GABA/metabolism , Receptors, N-Methyl-D-Aspartate/chemistry , Receptors, N-Methyl-D-Aspartate/metabolism , Signal Transduction , Up-Regulation/drug effects
3.
Mol Pain ; 14: 1744806918814367, 2018.
Article in English | MEDLINE | ID: mdl-30380983

ABSTRACT

Tetrahydroxystilbene glucoside (THSG) is one of the active ingredients of Polygonum multiflorum. It has been shown to exert a variety of pharmacological effects, including antioxidant, anti-aging, and anti-atherosclerosis. Because of its prominent anti-inflammatory effect, we explored whether THSG had analgesic effect. In this study, we used a model of chronic inflammatory pain caused by injecting complete Freund's adjuvant into the hind paw of mice. We found THSG relieved swelling and pain in the hind paw of mice on a dose-dependent manner. In the anterior cingulate cortex, THSG suppressed the upregulation of GluN2B-containing N-methyl-D-aspartate receptors and the downregulation of GluN2A-containing N-methyl-D-aspartate receptors caused by chronic inflammation. In addition, THSG increased Bcl-2 and decreased Bax and Caspase-3 expression by protecting neuronal survival. Furthermore, THSG inhibited the phosphorylation of p38 and the increase of nuclear factor κB (NF-κB) and tumor necrosis factor α (TNF-α). Immunohistochemical staining revealed that THSG blocked the activation of microglia and reduced the release of proinflammatory cytokines TNF-α, interleukin 1ß (IL-1ß), and interleukin 6 (IL-6). In conclusion, this study demonstrated that THSG had a certain effect on alleviating complete Freund's adjuvant-induced chronic inflammatory pain.


Subject(s)
Apoptosis , Chronic Pain/drug therapy , Glucosides/therapeutic use , Gyrus Cinguli/metabolism , Gyrus Cinguli/pathology , Inflammation/drug therapy , Microglia/pathology , Receptors, N-Methyl-D-Aspartate/metabolism , Stilbenes/therapeutic use , Animals , Apoptosis/drug effects , Cell Survival/drug effects , Chronic Pain/complications , Chronic Pain/pathology , Cytokines/metabolism , Edema/drug therapy , Freund's Adjuvant/administration & dosage , Glucosides/chemistry , Glucosides/pharmacology , Gyrus Cinguli/drug effects , Hyperalgesia/complications , Hyperalgesia/drug therapy , Inflammation/complications , Inflammation/pathology , Inflammation Mediators/metabolism , Male , Mice, Inbred C57BL , Microglia/drug effects , Microglia/metabolism , NF-kappa B/metabolism , Signal Transduction , Stilbenes/chemistry , Stilbenes/pharmacology , p38 Mitogen-Activated Protein Kinases/metabolism
4.
Biomed Pharmacother ; 86: 81-87, 2017 Feb.
Article in English | MEDLINE | ID: mdl-27939523

ABSTRACT

Huntington's disease (HD) is an autosomal dominant inherited disease characterized by movement, psychiatric, and cognitive disorders. Previous research suggests that Praeruptorin C (Pra-C), an effective component in the root of Peucedanum praeruptorum dunn, a traditional Chinese medicine, may function in neuroprotection. The present study was conducted to evaluate the effectiveness of Pra-C in the treatment of HD-like symptoms in a 3-nitropropionic acid (3-NP) mouse model, and to explore the possible mechanism of the drug's activity. We treated 3-NP-injected mice with two different doses of Pra-C (1.5 and 3.0mg/kg) for 3 days. Motor behavior was tested using the open field test (OFT) and rotarod test, while psychiatric symptoms were tested using the forced swimming test (FST) and tail suspension test (TST). We found that Pra-C alleviated the motor deficits and depression-like behavior in the 3-NP-treated mice, and protected neurons from excitotoxicity. Western blot analysis revealed that Pra-C upregulated BDNF, DARPP32, and huntingtin protein in the striatum of 3-NP mice. These results taken together suggest that Pra-C may have therapeutic potential with respect to the movement, psychiatric, and cognitive symptoms of HD.


Subject(s)
Coumarins/therapeutic use , Disease Models, Animal , Drugs, Chinese Herbal/therapeutic use , Huntington Disease/chemically induced , Huntington Disease/drug therapy , Nitro Compounds/toxicity , Propionates/toxicity , Animals , Dose-Response Relationship, Drug , Huntington Disease/metabolism , Mice , Mice, Inbred C57BL , Neuroprotective Agents/therapeutic use , Treatment Outcome
SELECTION OF CITATIONS
SEARCH DETAIL