7 results on '"Ji MH"'
Search Results
2. Histone deacetylase 3 in hippocampus contributes to memory impairment after chronic constriction injury of sciatic nerve in mice.
- Author
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Zhang GF, Zhou ZQ, Guo J, Gu HW, Su MZ, Yu BC, Zhou F, Han BY, Jia M, Ji MH, Tao YX, Zhao CJ, and Yang JJ
- Subjects
- Animals, Constriction, Mice, Sciatic Nerve metabolism, Hippocampus metabolism, Histone Deacetylases genetics, Histone Deacetylases metabolism
- Abstract
Abstract: Chronic neuropathic pain is frequently accompanied by memory impairment, yet the underlying mechanisms remain unclear. Here, we showed that mice displayed memory impairment starting at 14 days and lasting for at least 21 days after chronic constriction injury (CCI) of unilateral sciatic nerve in mice. Systemic administration of the pan histone deacetylase (HDAC) inhibitor sodium butyrate attenuated this memory impairment. More specifically, we found that hippocampus HDAC3 was involved in this process because the levels of its mRNA and protein increased significantly in the hippocampus at 14 and 21 days after CCI, but not sham surgery. Systemic administration of the selective HDAC3 antagonist RGFP966 attenuated CCI-induced memory impairment, improved hippocampal long-term potentiation impairment, and rescued reductions of dendritic spine density and synaptic plasticity-associated protein in the hippocampus. In addition, HDAC3 overexpression in the hippocampus led to memory impairment without affecting basal nociceptive responses in naive mice. Our findings suggest that HDAC3 contributes to memory impairment after CCI by impairing synaptic plasticity in hippocampus. Histone deacetylase 3 might serve as a potential molecular target for therapeutic treatment of memory impairment under neuropathic pain conditions., (Copyright © 2020 International Association for the Study of Pain.)
- Published
- 2021
- Full Text
- View/download PDF
3. Hippocampal complement C3 might contribute to cognitive impairment induced by anesthesia and surgery.
- Author
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Ji MH, Qiu LL, Mao MJ, Zhang L, and Yang JJ
- Subjects
- Aged, Animals, Complement C3 antagonists & inhibitors, Dendritic Spines drug effects, Gastrointestinal Diseases surgery, Humans, Male, Mice, Inbred C57BL, Neuropsychological Tests, Peptides, Cyclic administration & dosage, Postoperative Cognitive Complications blood, Proteomics, Up-Regulation, Anesthesia adverse effects, Anesthetics, Inhalation adverse effects, Complement C3 metabolism, Hippocampus drug effects, Hippocampus metabolism, Postoperative Cognitive Complications chemically induced, Postoperative Cognitive Complications metabolism, Sevoflurane administration & dosage
- Abstract
Postoperative cognitive dysfunction is a well-recognized complication after major surgery in the elderly, but its pathophysiological mechanism is not fully understood. In the present study, we used liquid chromatography-tandem mass spectrometry combined with tandem mass tags to identify differentially expressed proteins and perform further functional studies on protein of interest. Here, we showed that hippocampal complement C3 was significantly upregulated after surgery, which was accompanied by marked decreases in synaptic related proteins and density. In aged patients undergoing gastrointestinal surgery, we also found significantly increased plasma level of C3b postoperatively and were negatively associated with cognitive performance. Notably, selective inhibition of complement C3 by compstatin was able to rescue synaptic and cognitive impairments induced by surgery in aged mice. Collectively, our study confirms that surgery can induce cognitive impairments, and the possible mechanisms might be related to abnormal complement signaling and synaptic disruption.
- Published
- 2020
- Full Text
- View/download PDF
4. Ketamine differentially restores diverse alterations of neuroligins in brain regions in a rat model of neuropathic pain-induced depression.
- Author
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Pan W, Zhang GF, Li HH, Ji MH, Zhou ZQ, Li KY, and Yang JJ
- Subjects
- Animals, Brain-Derived Neurotrophic Factor metabolism, Depression metabolism, Disease Models, Animal, Gyrus Cinguli drug effects, Gyrus Cinguli metabolism, Hippocampus drug effects, Hippocampus metabolism, Hyperalgesia drug therapy, Hyperalgesia metabolism, Male, Neuralgia metabolism, Prefrontal Cortex drug effects, Prefrontal Cortex metabolism, Rats, Sprague-Dawley, Antidepressive Agents pharmacology, Behavior, Animal drug effects, Depression drug therapy, Ketamine pharmacology, Neuralgia drug therapy
- Abstract
Depression is present in a large proportion of patients suffering from chronic pain, and yet the underlying mechanisms remain to be elucidated. Neuroligins (NLs), as a family of cell-adhesion proteins, are involved in synaptic formation and have been linked to various neuropsychiatric disorders. Here, we studied the alterations in NL1 and NL2 in the medial prefrontal cortex (mPFC), the anterior cingulate cortex (ACC), and the hippocampus in a rat model of neuropathic pain-induced depression, and whether ketamine, a rapid and robust antidepressant, could restore these abnormalities. In the present study, we found that spared nerve injury induced significant mechanical allodynia and subsequent depressive-like symptoms, along with decreased NL1 and increased NL2 in the mPFC, decreased NL1 in the ACC, and decreased NL2 in the hippocampus. In addition, brain-derived neurotrophic factor (BDNF) was reduced in these brain regions. It is noteworthy that ketamine (10 mg/kg) relieved neuropathic pain-induced depressive behaviors and restored alterations of BDNF and NLs in the mPFC and the hippocampus at 24 h and 72 h after the administration of ketamine, but only restored BDNF in the ACC. In conclusion, NLs showed diverse changes in different brain regions in the rat model of neuropathic pain-induced depression, which could be reversed differentially by the administration of ketamine.
- Published
- 2018
- Full Text
- View/download PDF
5. Disruption of hippocampal neuregulin 1-ErbB4 signaling contributes to the hippocampus-dependent cognitive impairment induced by isoflurane in aged mice.
- Author
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Li XM, Su F, Ji MH, Zhang GF, Qiu LL, Jia M, Gao J, Xie Z, and Yang JJ
- Subjects
- Aging physiology, Animals, Blotting, Western, Down-Regulation drug effects, Enzyme-Linked Immunosorbent Assay, Exploratory Behavior drug effects, Fear psychology, Fluorescent Antibody Technique, Glutamate Decarboxylase biosynthesis, Injections, Intraventricular, Interneurons metabolism, Male, Mice, Mice, Inbred C57BL, Motor Activity drug effects, Parvalbumins biosynthesis, Parvalbumins metabolism, Receptor, ErbB-4, Signal Transduction drug effects, Anesthetics, Inhalation pharmacology, Cognition Disorders chemically induced, Cognition Disorders physiopathology, ErbB Receptors drug effects, Hippocampus physiopathology, Isoflurane pharmacology, Neuregulin-1 drug effects
- Abstract
Background: A prolonged isoflurane exposure may lead to cognitive decline in rodents. Neuregulin 1 (NRG1)-ErbB4 signaling plays a key role in the modulation of hippocampal synaptic plasticity through regulating the neurotransmission. The authors hypothesized that hippocampal NRG1-ErbB4 signaling is involved in isoflurane-induced cognitive impairments in aged mice., Methods: Fourteen-month-old C57BL/6 mice were randomized to receive 100% O2 exposure, vehicle injection after 100% O2 exposure, vehicle injection after exposure to isoflurane carried by 100% O2, NRG1-β1 injection after exposure to isoflurane carried by 100% O2, and NRG1-β1 and an ErbB4 inhibitor AG1478 injection after exposure to isoflurane carried by 100% O2. Fear conditioning test was used to assess the cognitive function of mice 48-h postexposure. The brain tissues were harvested 48-h postexposure to determine the levels of NRG1, ErbB4, p-ErbB4, parvalbumin, and glutamic acid decarboxylase 67 in the hippocampus using Western blotting, enzyme-linked immunosorbent assay, and immunofluorescence., Results: The percentage of freezing time to context was decreased from 50.28 ± 11.53% to 30.82 ± 10.00%, and the hippocampal levels of NRG1, p-ErbB4/ErbB4, parvalbumin, and glutamic acid decarboxylase 67 were decreased from 172.79 ± 20.85 ng/g, 69.15 ± 12.20%, 101.68 ± 11.21%, and 104.71 ± 6.85% to 112.92 ± 16.65 ng/g, 42.26 ± 9.71%, 75.89 ± 10.26%, and 73.87 ± 16.89%, respectively, after isoflurane exposure. NRG1-β1 attenuated the isoflurane-induced hippocampus-dependent cognitive impairment and the declines in the hippocampal NRG1, p-ErbB4/ErbB4, parvalbumin, and glutamic acid decarboxylase 67. AG1478 inhibited the rescuing effects of NRG1-β1., Conclusion: Disruption of NRG1-ErbB4 signaling in the parvalbumin-positive interneurons might, at least partially, contribute to the isoflurane-induced hippocampus-dependent cognitive impairment after exposure to isoflurane carried by 100% O2 in aged mice.
- Published
- 2014
- Full Text
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6. Blood pressure reduction induced by low dose of epinephrine via different routes in rats.
- Author
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Wu J, Ji MH, Wang ZY, Zhu W, Yang JJ, and Peng YG
- Subjects
- Administration, Intranasal, Adrenergic beta-2 Receptor Agonists adverse effects, Adrenergic beta-2 Receptor Agonists chemistry, Adrenergic beta-2 Receptor Antagonists therapeutic use, Animals, Antihypertensive Agents adverse effects, Antihypertensive Agents antagonists & inhibitors, Aorta, Thoracic, Epinephrine adverse effects, Epinephrine antagonists & inhibitors, Femoral Vein, Heart Rate drug effects, Hypotension chemically induced, Hypotension prevention & control, Infusions, Intra-Arterial, Infusions, Intravenous, Male, Propanolamines therapeutic use, Random Allocation, Rats, Rats, Sprague-Dawley, Receptors, Adrenergic, beta-2 chemistry, Receptors, Adrenergic, beta-2 metabolism, Adrenergic beta-2 Receptor Agonists administration & dosage, Antihypertensive Agents administration & dosage, Blood Pressure drug effects, Epinephrine administration & dosage
- Abstract
Background: Epinephrine was recently shown to induce a hypotension episode. Activation of β₂-adrenoceptors with smooth muscle relaxation may be the underlying mechanism. This study investigated the effects of ICI 118551, a β₂-adrenoceptors antagonist, on epinephrine-induced blood pressure reduction via different administration routes in rats., Methods: A total of 144 Sprague Dawley rats were equally randomized into 3 groups (intranasal, intravenous, and intra-arterial administration), each with 4 subgroups: saline + saline, ICI 118551 + saline, saline + epinephrine, and ICI 118551 + epinephrine. All rats were anesthetized while spontaneously breathing. Epinephrine was administered at doses of 5 μg/kg via nose, 0.25 μg/kg via femoral vein, and 0.1 μg/kg via aorta. Mean arterial pressure and heart rate were monitored., Results: Mean arterial pressure decreased in all 3 saline + epinephrine subgroups after administration (P < 0.05), whereas it did not in other subgroups. Heart rate had no significant change in all subgroups., Conclusions: Epinephrine-induced blood pressure reduction can be prevented by ICI 118551 in rats, suggesting that the activation of β₂-adrenoceptors contributes to blood pressure reduction.
- Published
- 2013
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7. Combined arginine vasopressin and levosimendan: a promising therapy for septic shock.
- Author
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Yang JJ, Wang X, Ji MH, and Peng YG
- Subjects
- Animals, Arginine Vasopressin administration & dosage, Drug Therapy, Combination, Humans, Hydrazones administration & dosage, Pyridazines administration & dosage, Sheep, Simendan, Vasodilator Agents administration & dosage, Arginine Vasopressin therapeutic use, Hydrazones therapeutic use, Pyridazines therapeutic use, Shock, Septic drug therapy, Vasodilator Agents therapeutic use
- Published
- 2011
- Full Text
- View/download PDF
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