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Your search keyword '"Li, Junfa"' showing total 9 results
Start Over Author "Li, Junfa" Journal journal of neurosurgical anesthesiology
9 results on '"Li, Junfa"'

3. nPKCϵ and NMDA Receptors Participate in Neuroprotection Induced by Morphine Pretreatment

Author

Ji Fang, Li Junfa, Meng Fanjun, and Zhang Bingxi

Subjects
Male, Blotting, Western, Nerve Tissue Proteins, Protein Kinase C-epsilon, Pharmacology, Receptors, N-Methyl-D-Aspartate, Neuroprotection, Mice, chemistry.chemical_compound, Cytosol, medicine, Animals, Phosphorylation, Hypoxia, Receptor, Protein kinase C, Neurons, Mice, Inbred BALB C, Dose-Response Relationship, Drug, Morphine, business.industry, Antagonist, Analgesics, Opioid, Glucose, Neuroprotective Agents, Anesthesiology and Pain Medicine, Chelerythrine, chemistry, NMDA receptor, Electrophoresis, Polyacrylamide Gel, Female, Surgery, Neurology (clinical), business, medicine.drug
Abstract

Morphine pretreatment induces ischemic tolerance in neurons, but it remains uncertain whether novel protein kinase C epsilon isoform (nPKCepsilon) and N-methyl-D-aspartate (NMDA) receptors are involved in this neuroprotection. The present study examined this issue. Hippocampal slices from adult BALB/C mice were incubated with morphine at 0.1-10.0 muM in the presence or absence of various antagonists for 30 minutes and then kept in morphine- and antagonist-free buffer for 30 minutes before being subjected to oxygen-glucose deprivation for 20 minutes. After recovery in oxygenated artificial fluid for 5 hours, assessment of slice injury was done by determination of the intensity of slice stain after they were incubated with 2% 2,3,5-triphenyltetrazolium chloride for 30 minutes and extracted by organic solvent for 24 hours. At designated periods, slices were preserved for immunoblot analysis to observe effects of morphine pretreatment on membrane translocation and total protein expression of nPKCepsilon and phosphorylation of NR1 subunits of NMDA receptors. The neuroprotection induced by morphine pretreatment was partially blocked by chelerythrine (a nonselective PKC blocker), epsilonv(1-2) (a selective nPKCepsilon antagonist), MK-801 (a noncompetitive NMDA receptor blocker), chelerythrine combined with MK-801, and epsilonv(1-2) with MK-801. Morphine pretreatment significantly inhibited nPKCepsilon membrane translocation and phosphorylation of NR1 subunits of NMDA receptors during reperfusion injury. However, epsilonv(1-2) blocked these effects induced by morphine pretreatment. These findings suggested that nPKCepsilon and NMDA receptors might participate in neuroprotection induced by morphine pretreatment, and NMDA receptors might be downstream targets of nPKCepsilon.

Published
2006

9. Morphine Preconditioning Alleviates Ischemia/Reperfusion-induced Caspase-8-dependent Neuronal Apoptosis through cPKCγ-NF-κB-cFLIPL Pathway.

Author

Huang Y, Chi W, Li Y, Zhang C, Li J, and Meng F

Abstract

Background: Perioperative cerebral ischemia/reperfusion injury is a major contributor to postoperative death and cognitive dysfunction in patients. It was reported that morphine preconditioning (MP) can mimic ischemia/hypoxia preconditioning to protect against ischemia/reperfusion injury. However, the mechanism of MP on the ischemia/reperfusion-induced neuronal apoptosis has not been fully clarified., Methods: The middle cerebral artery occlusion/reperfusion (MCAO/R) model of mice and the oxygen-glucose deprivation/reoxygenation (OGD/R) model in primary cortical neurons were used to mimic ischemic stroke. In vivo, the infarct size was measured by using TTC staining; NDSS, Longa score system, and beam balance test were performed to evaluate the neurological deficits of mice; the expression of the protein was detected by using a western blot. In vitro, the viability of neurons was determined by using CCK-8 assay; the expression of protein and mRNA were assessed by using western blot, RT-qPCR, and immunofluorescent staining; the level of apoptosis was detected by using TUNEL staining., Results: MP can improve the neurological functions of mice following MCAO/R (P<0.001, n=10 per group). MP can decrease the infarct size (P<0.001, n=10 per group) and the level of cleaved-caspase-3 of mice following MCAO/R (P<0.01 or 0.001, n=6 per group). MP can increase the levels of cPKCγ membrane translocation, p-p65, and cFLIPL, and decrease the levels of cleaved-caspase-8, 3 in neurons after OGD/R or MCAO/R 1 d (P<0.05, 0.01 or 0.001, n=6 per group). In addition, MP could alleviate OGD/R-induced cell apoptosis (P<0.001, n=6 per group)., Conclusion: MP alleviates ischemia/reperfusion-induced Caspase 8-dependent neuronal apoptosis through the cPKCγ-NF-κB-cFLIPL pathway., Competing Interests: The authors have no conflicts of interest to disclose., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

Published
2024
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