Objective: , is a traditional Chinese medicine commonly employed for pain management. However, its primary active ingredient remains a subject of debate.
Methods: Spinal nerve ligation (SNL) and formalin-induced pain models were employed. Network pharmacology and bioinformatics were utilized to identify targets. Verification was performed through spinal cord double immunofluorescence staining, quantitative PCR and whole-cell recording techniques.
Results: In experiments conducted on neuropathic rats, both systemic and intrathecal administration of astilbin, an essential constituent, exhibited a noteworthy and dose-dependently decrease in chronic and acute pain behaviours. The ED value, which represents the dose at which 50% effectiveness is achieved, was measure at 7.59 μg, while the value, indicating the maximum attainable effect, was found to be 60% of the maximal possible effect (% MPE). Forty-two shared targets were identified, enriching the metabolic and synaptic pathways in the network pharmacology analysis, as confirmed by transcriptomic analysis. Weighted gene co-expression network analysis (WGCNA) revealed a strong correlation between the anti-nociceptive effects of astilbin and neuronal metabolic processes. Spinal functional ultrasound (FUS) analysis indicated increased spinal blood flow intensity and changes in metabolism-related enzyme activity, including stearoyl-CoA desaturase (), 17beta-hydroxysteroid dehydrogenase () and sterol 14alpha-demethylase () in neuropathic rats, pretreatment with astilbin decreased formalin-induced blood flow in acute pain. Bath application of astilbin dose-dependently inhibited neuronal activity by reducing the frequency and amplitude of miniature excitatory postsynaptic currents (mEPSCs) without affecting miniature inhibitory postsynaptic currents (mIPSCs).
Conclusions: In summary, this study provides evidence that astilbin alleviates pain by modulating neuronal metabolic processes and synaptic homeostasis.
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http://dx.doi.org/10.1080/07853890.2024.2396561 | DOI Listing |
Mol Neurobiol
December 2024
Department of neurology, The Third Affiliated Hospital, Sun Yat-sen University, 600 Tianhe Road, Guangzhou, 510630, Guangdong, China.
Aims: This study aims to elucidate the therapeutic effects and underlying mechanisms of exosomes derived from Heme oxygenase 1 (HO-1)-overexpressing human umbilical cord mesenchymal stem cells (Exo) in a subarachnoid hemorrhage (SAH) mouse model.
Methods: In this study, exosomes were identified using Western blotting, particle analysis, and transmission electron microscopy. The effect of Exo and Exo on the neurological function of SAH mice was assessed using the Garcia scoring system, Beam balance, Rotarod test, and Morris water maze test.
Psychopharmacology (Berl)
December 2024
Department of Psychosis Studies, Institute of Psychiatry, Psychology & Neuroscience, Kings College London, De Crespigny Park, London, SE5 8AF, UK.
Rationale: Working memory impairment is a prominent feature of schizophrenia which predicts clinical and functional outcomes. Preclinical data suggest histamine-3 receptor (H3R) expression in cortical pyramidal neurons may have a role in working memory, and post-mortem data has found disruptions of H3R expression in schizophrenia.
Objectives: We examined the role of H3R in vivo to elucidate its role on working memory impairment in schizophrenia.
Exp Neurol
December 2024
Center for Integrative Brain Research, Seattle Children's Research Institute, Seattle, WA 98101, United States of America; Department of Neurological Surgery, University of Washington School of Medicine, Seattle, WA 98108, USA. Electronic address:
Swallowing, both nutritive and non-nutritive, is highly dysfunctional in children with Leigh Syndrome (LS) and contributes to the need for both gastrostomy and tracheostomy tube placement. Without these interventions aspiration of food, liquid, and mucus occur resulting in repeated bouts of respiratory infection. No study has investigated whether mouse models of LS, a neurometabolic disorder, exhibit dysfunctions in neuromuscular activity of swallow and breathing integration.
View Article and Find Full Text PDFExp Neurol
December 2024
Neuroscience Department, U.S. Army Medical Research Institute of Chemical Defense (USAMRICD), Aberdeen Proving Ground, MD, United States of America. Electronic address:
Exposure to organophosphorus nerve agents irreversibly inhibits acetylcholinesterase and may lead to cholinergic crisis and seizures. Although benzodiazepines are the standard of care after nerve agent-induced status epilepticus, when treatment is delayed for up to 30 min or more, refractory status epilepticus can develop. Adult male rodents are often utilized for evaluation of therapeutic efficacy against nerve agent exposure.
View Article and Find Full Text PDFJ Ethnopharmacol
December 2024
Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, China; Science and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou 510405, Guangdong, China; Institute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, China; State Key Laboratory of Dampness Syndrome of Chinese Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, China. Electronic address:
Ethnopharmacological Relevance: Delayed tissue-type plasminogen activator (t-PA) thrombolysis, which has a restrictive therapeutic time window within 4.5 h following ischemic stroke (IS), increases the risk of hemorrhagic transformation (HT) and subsequent neurotoxicity. Studies have shown that the NLRP3 inflammasome activation reversely regulated by the PGC-1α leads to microglial polarization and pyroptosis to cause damage to nerve cells and the blood-brain barrier.
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