43 results on '"Zong-yong Zhang"'
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2. Retraction of 'Ravoxertinib Improves Long-Term Neurologic Deficits after Experimental Subarachnoid Hemorrhage through Early Inhibition of Erk1/2'
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Ming-feng Yang, Sheng-yao Sun, Hai-guang Lv, Wei-qi Wang, Han-xia Li, Jing-yi Sun, and Zong-yong Zhang
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Chemistry ,QD1-999 - Published
- 2024
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3. RETRACTED: Ravoxertinib Improves Long-Term Neurologic Deficits after Experimental Subarachnoid Hemorrhage through Early Inhibition of Erk1/2
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Ming-feng Yang, Sheng-yao Sun, Hai-guang Lv, Wei-qi Wang, Han-xia Li, Jing-yi Sun, and Zong-yong Zhang
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Chemistry ,QD1-999 - Published
- 2023
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4. TAT-HSP27 Peptide Improves Neurologic Deficits via Reducing Apoptosis After Experimental Subarachnoid Hemorrhage
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Xiao-yan Zhou, Jing-yi Sun, Wei-qi Wang, Shu-xian Li, Han-xia Li, Hui-juan Yang, Ming-feng Yang, Hui Yuan, Zong-yong Zhang, Bao-liang Sun, and Jin-Xiang Han
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subarachnoid hemorrhage ,HSP27 ,cell apoptosis ,neurologic deficits ,TAT-HSP2765−90 peptide ,Neurosciences. Biological psychiatry. Neuropsychiatry ,RC321-571 - Abstract
Cell apoptosis plays an important role in early brain injury (EBI) after subarachnoid hemorrhage (SAH). Heat shock protein 27 (HSP27), a member of the small heat shock protein (HSP) family, is induced by various stress factors and exerts protective role on cells. However, the role of HSP27 in brain injury after SAH needs to be further clarified. Here, we reported that HSP27 level of cerebrospinal fluid (CSF) is increased obviously at day 1 in patients with aneurysmal SAH (aSAH) and related to the grades of Hunt and Hess (HH), World Federation of Neurological Surgeons (WFNS), and Fisher score. In rat SAH model, HSP27 of CSF is first increased and then obviously declined; overexpression of HSP27, not knockdown of HSP27, attenuates SAH-induced neurological deficit and cell apoptosis in the basal cortex; and overexpression of HSP27 effectively suppresses SAH-elevated activation of mitogen-activated protein Kinase Kinase 4 (MKK4), the c-Jun N-terminal kinase (JNK), c-Jun, and caspase-3. In an in vitro hemolysate-damaged cortical neuron model, HSP2765−90 peptide effectively inhibits hemolysate-induced neuron death. Furthermore, TAT-HSP2765−90 peptide, a fusion peptide consisting of trans-activating regulatory protein (TAT) of HIV and HSP2765−90 peptide, effectively attenuates SAH-induced neurological deficit and cell apoptosis in the basal cortex of rats. Altogether, our results suggest that TAT-HSP27 peptide improves neurologic deficits via reducing apoptosis.
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- 2022
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5. Early High Cerebrospinal Fluid Glutamate: A Potential Predictor for Delayed Cerebral Ischemia after Aneurysmal Subarachnoid Hemorrhage
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Hong-Bin Wang, Qing-Jian Wu, Shi-jun Zhao, Ya-jun Hou, Han-xia Li, Ming-feng Yang, Bao-Jun Wang, Bao-liang Sun, and Zong-yong Zhang
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Chemistry ,QD1-999 - Published
- 2020
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6. Selenocysteine induces apoptosis in human glioma cells: evidence for TrxR1-targeted inhibition and signaling crosstalk
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Cun-dong Fan, Xiao-yan Fu, Zong-yong Zhang, Ming-zhi Cao, Jing-yi Sun, Ming-feng Yang, Xiao-ting Fu, Shi-jun Zhao, Lu-rong Shao, Hui-fang Zhang, Xiao-yi Yang, and Bao-liang Sun
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Medicine ,Science - Abstract
Abstract Thioredoxin reductase (TrxR) as a selenium (Se)-containing antioxidase plays key role in regulating intracellular redox status. Selenocystine (SeC) a natural available Se-containing amino acid showed novel anticancer potential through triggering oxidative damage-mediated apoptosis. However, whether TrxR-mediated oxidative damage was involved in SeC-induced apoptosis in human glioma cells has not been elucidated yet. Herein, SeC-induced human glioma cell apoptosis was detected in vitro, accompanied by PARP cleavage, caspases activation and DNA fragmentation. Mechanically, SeC caused mitochondrial dysfunction and imbalance of Bcl-2 family expression. SeC treatment also triggered ROS-mediated DNA damage and disturbed the MAPKs and AKT pathways. However, inhibition of ROS overproduction effectively attenuated SeC-induced oxidative damage and apoptosis, and normalized the expression of MAPKs and AKT pathways, indicating the significance of ROS in SeC-induced apoptosis. Importantly, U251 human glioma xenograft growth in nude mice was significantly inhibited in vivo. Further investigation revealed that SeC-induced oxidative damage was achieved by TrxR1-targeted inhibition in vitro and in vivo. Our findings validated the potential of SeC to inhibit human glioma growth by oxidative damage-mediated apoptosis through triggering TrxR1-targeted inhibition.
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- 2017
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7. TAT-HSP27 Peptide Improves Neurologic Deficits via Reducing Apoptosis After Experimental Subarachnoid Hemorrhage.
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Xiao-yan Zhou, Jing-yi Sun, Wei-qi Wang, Shu-xian Li, Han-xia Li, Hui-juan Yang, Ming-feng Yang, Hui Yuan, Zong-yong Zhang, Bao-liang Sun, and Jin-Xiang Han
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PEPTIDES ,SUBARACHNOID hemorrhage ,MITOGENS ,RHINORRHEA ,CELL death ,HEAT shock proteins ,APOPTOSIS ,MITOGEN-activated protein kinases ,LABORATORY rats - Abstract
Cell apoptosis plays an important role in early brain injury (EBI) after subarachnoid hemorrhage (SAH). Heat shock protein 27 (HSP27), a member of the small heat shock protein (HSP) family, is induced by various stress factors and exerts protective role on cells. However, the role of HSP27 in brain injury after SAH needs to be further clarified. Here, we reported that HSP27 level of cerebrospinal fluid (CSF) is increased obviously at day 1 in patients with aneurysmal SAH (aSAH) and related to the grades of Hunt and Hess (HH), World Federation of Neurological Surgeons (WFNS), and Fisher score. In rat SAH model, HSP27 of CSF is first increased and then obviously declined; overexpression of HSP27, not knockdown of HSP27, attenuates SAH-induced neurological deficit and cell apoptosis in the basal cortex; and overexpression of HSP27 effectively suppresses SAH-elevated activation of mitogen-activated protein Kinase Kinase 4 (MKK4), the c-Jun N-terminal kinase (JNK), c-Jun, and caspase-3. In an in vitro hemolysate-damaged cortical neuron model, HSP2765−90 peptide effectively inhibits hemolysate-induced neuron death. Furthermore, TAT-HSP27
65−90 peptide, a fusion peptide consisting of trans-activating regulatory protein (TAT) of HIV and HSP2765−90 peptide, effectively attenuates SAH-induced neurological deficit and cell apoptosis in the basal cortex of rats. Altogether, our results suggest that TAT-HSP27 peptide improves neurologic deficits via reducing apoptosis. [ABSTRACT FROM AUTHOR]- Published
- 2024
- Full Text
- View/download PDF
8. The prognostic value of hyperglycemia in aneurysmal subarachnoid hemorrhage: a systematic review and meta-analysis
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Min, Shi, Ting-Bao, Zhang, Xiao-Feng, Li, Zong-Yong, Zhang, Ze-Jin, Li, Xue-Lou, Wang, and Wen-Yuan, Zhao
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Hyperglycemia ,Humans ,Vasospasm, Intracranial ,Surgery ,Cerebral Infarction ,Neurology (clinical) ,General Medicine ,Subarachnoid Hemorrhage ,Prognosis - Abstract
Recent studies have demonstrated that hyperglycemia may result in a poor prognosis following aneurysmal subarachnoid hemorrhage (aSAH). However, the association between hyperglycemia and the clinical outcome of aSAH has not been clearly established thus far. Therefore, we performed a systematic review and meta-analysis to investigate the association between hyperglycemia and the development of aSAH. We completed a literature search in four databases (PubMed, EMBASE, Cochrane Library, and Web of Science) up to November 1, 2021, including all eligible studies investigating the prognostic value of hyperglycemia in patients with aSAH. We performed a quality assessment of included studies using the Newcastle-Ottawa Quality Assessment Scale. The pooled odds ratios (ORs) with corresponding 95% confidence intervals (CIs) were calculated to assess the association of hyperglycemia in aneurysmal subarachnoid hemorrhage. A total of 35 studies with 11,519 patients were finally included in the meta-analysis. Nineteen studies reported the association between hyperglycemia and poor outcome, 12 studies reported the association between hyperglycemia and all-cause mortality, 7 studies reported the association between hyperglycemia and cerebral vasospasm, and 9 studies reported the association between hyperglycemia and cerebral infarction. The pooled data of these studies suggested that hyperglycemia was significantly associated with poor functional outcomes (odds ratio [OR], 1.29; 95% confidence interval [CI], 1.17-1.42; P 0.00001; I
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- 2022
9. Ravoxertinib Improves Long-Term Neurologic Deficits after Experimental Subarachnoid Hemorrhage through Early Inhibition of Erk1/2
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Ming-feng Yang, Sheng-yao Sun, Hai-guang Lv, Wei-qi Wang, Han-xia Li, Jing-yi Sun, and Zong-yong Zhang
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General Chemical Engineering ,General Chemistry - Published
- 2023
10. Diiron propane-1,2-dithiolate complexes with monosubstituted cyclohexyldiphenylphosphine or dicyclohexylphenylphosphine: synthesis, characterization, and X-ray crystallography
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Ming-Gang Wu, Zong-Yong Zhang, Xu-Feng Liu, Xing-Hai Liu, and Zhong-Qing Jiang
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General Materials Science ,General Chemistry ,Condensed Matter Physics - Published
- 2022
11. Ifenprodil Improves Long-Term Neurologic Deficits Through Antagonizing Glutamate-Induced Excitotoxicity After Experimental Subarachnoid Hemorrhage
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Hong-Bin Wang, Qingbin Ni, Qiong-Jie Mi, Jing-yi Sun, Shi-jun Zhao, Zong-yong Zhang, Ming-feng Yang, Ya-jun Hou, Hui Yuan, and Baoliang Sun
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0301 basic medicine ,Excitotoxicity ,Glutamic Acid ,Brain damage ,medicine.disease_cause ,Receptors, N-Methyl-D-Aspartate ,Cerebral edema ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Piperidines ,Ifenprodil ,Animals ,Humans ,Medicine ,business.industry ,General Neuroscience ,Glutamate receptor ,Human brain ,Subarachnoid Hemorrhage ,medicine.disease ,Rats ,030104 developmental biology ,medicine.anatomical_structure ,chemistry ,Blood-Brain Barrier ,NMDA receptor ,Neurology (clinical) ,medicine.symptom ,Basal cortex ,Cardiology and Cardiovascular Medicine ,business ,Neuroscience ,030217 neurology & neurosurgery - Abstract
Excessive glutamate leading to excitotoxicity worsens brain damage after SAH and contributes to long-term neurological deficits. The drug ifenprodil is a non-competitive antagonist of GluN1-GluN2B N-methyl-d-aspartate (NMDA) receptor, which mediates excitotoxic damage in vitro and in vivo. Here, we show that cerebrospinal fluid (CSF) glutamate level within 48 h was significantly elevated in aSAH patients who later developed poor outcome. In rat SAH model, ifenprodil can improve long-term sensorimotor and spatial learning deficits. Ifenprodil attenuates experimental SAH-induced neuronal death of basal cortex and hippocampal CA1 area, cellular and mitochondrial Ca2+ overload of basal cortex, blood-brain barrier (BBB) damage, and cerebral edema of early brain injury. Using in vitro models, ifenprodil declines the high-concentration glutamate-mediated intracellular Ca2+ increase and cell apoptosis in primary cortical neurons, reduces the high-concentration glutamate-elevated endothelial permeability in human brain microvascular endothelial cell (HBMEC). Altogether, our results suggest ifenprodil improves long-term neurologic deficits through antagonizing glutamate-induced excitotoxicity.
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- 2021
12. Tris(2-thienyl)phosphine-substituted diiron propanedithiolate complexes: Synthesis, spectroscopy, crystal structures, electrochemistry, and fungicidal activity
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Zong-Yong Zhang, Xing-Hai Liu, Lin Yan, Yu-Long Li, Jun Yang, and Xu-Feng Liu
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Tris ,010405 organic chemistry ,Organic Chemistry ,Crystal structure ,010402 general chemistry ,Electrochemistry ,01 natural sciences ,Biochemistry ,Medicinal chemistry ,0104 chemical sciences ,Inorganic Chemistry ,chemistry.chemical_compound ,chemistry ,Propanedithiolate ,Cyclic voltammetry ,Spectroscopy ,Phosphine - Abstract
In this article, we report two diiron propanedithiolate complexes with monosubstituted tris(2-thienyl)phosphine. Reaction of [Fe2(CO)6{μ-SCH2CH2CH2S}] (1) or [Fe2(CO)6{μ-SCH2CH(CH3)S}] (2) with one...
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- 2020
13. The novel Nrf2 activator CDDO‐EA attenuates cerebral ischemic injury by promoting microglia/macrophage polarization toward M2 phenotype in mice
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Leilei Mao, Zong-yong Zhang, Huayang Zhao, Xia Lei, Dong Qiwei, Min Li, Baoliang Sun, and Hanxia Li
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0301 basic medicine ,Male ,NF-E2-Related Factor 2 ,medicine.medical_treatment ,Intraperitoneal injection ,HO‐1 ,Stimulation ,Pharmacology ,Neuroprotection ,cerebral ischemia ,Nrf2 ,Brain Ischemia ,03 medical and health sciences ,chemistry.chemical_compound ,Mice ,0302 clinical medicine ,Physiology (medical) ,medicine ,Animals ,Pharmacology (medical) ,Oleanolic Acid ,Heme ,Cells, Cultured ,CDDO‐EA ,Microglia ,Macrophages ,Ischemic injury ,Original Articles ,Mice, Inbred C57BL ,Psychiatry and Mental health ,Cytosol ,030104 developmental biology ,medicine.anatomical_structure ,Phenotype ,chemistry ,Apoptosis ,microglia/macrophage ,Original Article ,030217 neurology & neurosurgery - Abstract
The aim of present study was to explore whether 2‐cyano‐3, 12‐dioxooleana‐1, 9‐dien‐28‐oic acid (CDDO)‐ethylamide (CDDO‐EA) attenuates cerebral ischemic injury and its possible mechanisms using a middle cerebral artery occlusion (MCAO) model in C57BL/6 mice. Our results showed that intraperitoneal injection (i.p.) of CDDO‐EA (2 and 4 mg/kg) augmented NFE2‐related factor 2 (Nrf2) and heme oxygenase‐1 (HO‐1) expression in ischemic cortex after MCAO. Moreover, CDDO‐EA (2 mg/kg, i.p.) significantly enhanced Nrf2 nuclear accumulation, associated with increased cytosolic HO‐1 expression, reduced neurological deficit and infarct volume as well as neural apoptosis, and shifted polarization of microglia/macrophages toward an antiinflammatory M2 phenotype in ischemic cortex after MCAO. Using an in vitro model, we confirmed that CDDO‐EA (100 μg/mL) increased HO‐1 expression and primed microglial polarization toward M2 phenotype under inflammatory stimulation in BV2 microglial cells. These findings suggest that a novel Nrf2 activator CDDO‐EA confers neuroprotection against ischemic injury.
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- 2020
14. Negative Allosteric Modulator of mGluR1 Improves Long-Term Neurologic Deficits after Experimental Subarachnoid Hemorrhage
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Hong-Bin Wang, Ya-jun Hou, Zong-yong Zhang, Qing-Jian Wu, Ming-feng Yang, Baoliang Sun, Hui-Juan Yang, Wei-Qi Wang, and Hanxia Li
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medicine.medical_specialty ,Allosteric modulator ,Subarachnoid hemorrhage ,Physiology ,Cognitive Neuroscience ,Perforation (oil well) ,Receptors, Metabotropic Glutamate ,Biochemistry ,03 medical and health sciences ,0302 clinical medicine ,Cerebral vasospasm ,Enos ,Internal medicine ,Animals ,Vasospasm, Intracranial ,Medicine ,cardiovascular diseases ,030304 developmental biology ,0303 health sciences ,biology ,business.industry ,Cell Biology ,General Medicine ,Subarachnoid Hemorrhage ,Neurovascular bundle ,biology.organism_classification ,medicine.disease ,Rats ,nervous system diseases ,Disease Models, Animal ,Cerebral blood flow ,Cardiology ,Metabotropic glutamate receptor 1 ,business ,030217 neurology & neurosurgery - Abstract
Aneurysmal subarachnoid hemorrhage (SAH) causes permanent neurological sequelae, but the underlying mechanism needs to be further clarified. Here, we show that inhibition of metabotropic glutamate receptor 1 (mGluR1) with negative allosteric modulator JNJ16259685 improves long-term neurobehavioral outcomes in an endovascular perforation model of SAH. JNJ16259685 improves cerebrovascular dysfunction through attenuation of cerebral blood flow (CBF) reduction, cerebral vasoconstrictio, and microthrombosis formation in a rat SAH model. Moreover, JNJ16259685 reduces experimental SAH-induced long-term neuronal damage through alleviation of neuronal death and degeneration. Mechanically, JNJ16259685 maintains phosphorylation of endothelial NO synthase (eNOS) and vasodilator-stimulated phosphoprotein (VASP) and decreases apoptosis-related factors Bax, active caspase-9, and active caspase-3 following experimental SAH. Altogether, our results suggest JNJ16259685 improves long-term functional impairment through neurovascular protection.
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- 2020
15. Early High Cerebrospinal Fluid Glutamate: A Potential Predictor for Delayed Cerebral Ischemia after Aneurysmal Subarachnoid Hemorrhage
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Zong-yong Zhang, Baojun Wang, Hanxia Li, Shi-jun Zhao, Ming-feng Yang, Qing-Jian Wu, Baoliang Sun, Hong-Bin Wang, and Ya-jun Hou
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Subarachnoid hemorrhage ,business.industry ,General Chemical Engineering ,Significant difference ,Glutamate receptor ,Ischemia ,General Chemistry ,medicine.disease ,Article ,Chemistry ,Cerebrospinal fluid ,Normal pressure hydrocephalus ,Anesthesia ,medicine ,Prospective clinical study ,business ,Complication ,QD1-999 - Abstract
Delayed cerebral ischemia (DCI) is an important complication after aneurysmal subarachnoid hemorrhage (aSAH). Early identification of cerebrospinal fluid (CSF) markers is helpful for warning of impending DCI. This study assessed whether early high CSF glutamate levels can be observed in aSAH patients who later developed DCI. In this prospective clinical study, patients with normal pressure hydrocephalus or aSAH were enrolled. We found that the early CSF levels of glutamate were significantly elevated in aSAH patients compared to patients with normal pressure hydrocephalus. There was a significant difference in early CSF levels of glutamate between aSAH patients without DCI and with DCI. The early CSF levels of glutamate are significantly related to the Hunt and Hess grade, the World Federation of Neurological Surgeons (WFNS) grade, and the modified Fisher score on admission and occurrence of DCI in aSAH patients. Preliminary evidence of this study suggests that early high CSF glutamate levels are correlated with DCI in aSAH patients.
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- 2020
16. Selective mGluR1 Negative Allosteric Modulator Reduces Blood–Brain Barrier Permeability and Cerebral Edema After Experimental Subarachnoid Hemorrhage
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Cheng Zhang, Zong-yong Zhang, Bao-liang Sun, Yan-Xin Yin, Ming Jiang, Shi-jun Zhao, Yu-Qiang Song, Qiong-Jie Mi, Ming-feng Yang, and Wei-Qi Wang
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0301 basic medicine ,Subarachnoid hemorrhage ,business.industry ,General Neuroscience ,Glutamate receptor ,Human brain ,Pharmacology ,medicine.disease ,Occludin ,Blood–brain barrier ,nervous system diseases ,Cerebral edema ,03 medical and health sciences ,030104 developmental biology ,0302 clinical medicine ,Cerebrospinal fluid ,medicine.anatomical_structure ,cardiovascular system ,medicine ,Metabotropic glutamate receptor 1 ,cardiovascular diseases ,Neurology (clinical) ,Cardiology and Cardiovascular Medicine ,business ,030217 neurology & neurosurgery - Abstract
The blood–brain barrier (BBB) disruption leads to the vasogenic brain edema and contributes to the early brain injury (EBI) after subarachnoid hemorrhage (SAH). However, the mechanisms underlying the BBB damage following SAH are poorly understood. Here we reported that the neurotransmitter glutamate of cerebrospinal fluid (CSF) was dramatically increased in SAH patients with symptoms of cerebral edema. Using the rat SAH model, we found that SAH caused the increase of CSF glutamate level and BBB permeability in EBI, intracerebroventricular injection of exogenous glutamate deteriorated BBB damage and cerebral edema, while intraperitoneally injection of metabotropic glutamate receptor 1(mGluR1) negative allosteric modulator JNJ16259685 significantly attenuated SAH-induced BBB damage and cerebral edema. In an in vitro BBB model, we showed that glutamate increased monolayer permeability of human brain microvascular endothelial cells (HBMEC), whereas JNJ16259685 preserved glutamate-damaged BBB integrity in HBMEC. Mechanically, glutamate downregulated the level and phosphorylation of vasodilator-stimulated phosphoprotein (VASP), decreased the tight junction protein occludin, and increased AQP4 expression at 72 h after SAH. However, JNJ16259685 significantly increased VASP, p-VASP, and occludin, and reduced AQP level at 72 h after SAH. Altogether, our results suggest an important role of glutamate in disruption of BBB function and inhibition of mGluR1 with JNJ16259685 reduced BBB damage and cerebral edema after SAH.
- Published
- 2019
17. TAT-mGluR1 Attenuation of Neuronal Apoptosis through Prevention of MGluR1α Truncation after Experimental Subarachnoid Hemorrhage
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Qiong-Jie Mi, Cheng Zhang, Rongxia Xie, Baoliang Sun, Zong-yong Zhang, Ping Han, Ming-feng Yang, and Weiqi Wang
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Male ,Subarachnoid hemorrhage ,Physiology ,Cognitive Neuroscience ,Apoptosis ,Peptide ,Pharmacology ,Receptors, Metabotropic Glutamate ,Biochemistry ,Rats, Sprague-Dawley ,03 medical and health sciences ,0302 clinical medicine ,Downregulation and upregulation ,medicine ,Animals ,cardiovascular diseases ,030304 developmental biology ,Neurons ,chemistry.chemical_classification ,Regulation of gene expression ,0303 health sciences ,biology ,Calpain ,Chemistry ,Cell Biology ,General Medicine ,Subarachnoid Hemorrhage ,medicine.disease ,nervous system diseases ,Neuroprotective Agents ,biology.protein ,Metabotropic glutamate receptor 1 ,Basal cortex ,030217 neurology & neurosurgery ,Signal Transduction - Abstract
Excessive glutamate-mediated overactivation of metabotropic glutamate receptor 1 (mGluR1) plays a leading role in neuronal apoptosis following subarachnoid hemorrhage (SAH). TAT-mGluR1, a fusion peptide consisting of a peptide spanning the calpain cleavage site of mGluR1α and the trans-activating regulatory protein (TAT) of HIV, effectively blocks mGluR1α truncation and protects neurons against excitotoxic damage. This study investigated the effects of TAT-mGluR1 on neuronal apoptosis in the rat SAH model. Here, we report that SAH caused activation of calpain and truncation of mGluR1α; intraperitoneally administered TAT-mGluR1 did not affect calpain activity, while it blocked truncation of mGluR1α after SAH. Intraperitoneally administered FITC-labeled TAT-mGluR1 was colocalized with mGluR1α in thecortex after SAH. Furthermore, TAT-mGluR1 significantly improved the neurological deficit, increased p-PI3K, p-Akt, and p-GSK3β, downregulated Bax, upregulated Bcl-2, and reduced cortical apoptosis in the basal cortex at 24 h after SAH. These findings indicated that TAT-mGluR1 acted against SAH-induced cell apoptosis through preventing mGluR1α truncation.
- Published
- 2018
18. The GluN1/GluN2B NMDA receptor and metabotropic glutamate receptor 1 negative allosteric modulator has enhanced neuroprotection in a rat subarachnoid hemorrhage model
- Author
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Jing-yi Sun, Bao-liang Sun, Ming-feng Yang, Xiao-yi Yang, Jian Wang, Zong-yong Zhang, Jiming Kong, Junke Liu, Siluo Huang, Hui Yuan, Rongxia Xie, Suyun Wang, Leilei Mao, and Cun-Dong Fan
- Subjects
0301 basic medicine ,Allosteric modulator ,Excitotoxicity ,Apoptosis ,Pharmacology ,Receptors, Metabotropic Glutamate ,medicine.disease_cause ,Receptors, N-Methyl-D-Aspartate ,Neuroprotection ,Rats, Sprague-Dawley ,Mice ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Piperidines ,Developmental Neuroscience ,Ifenprodil ,medicine ,Animals ,Receptor ,Adrenergic alpha-Antagonists ,Neurons ,Glutamate receptor ,Brain ,Subarachnoid Hemorrhage ,Rats ,Disease Models, Animal ,Neuroprotective Agents ,030104 developmental biology ,Neurology ,chemistry ,Quinolines ,Metabotropic glutamate receptor 1 ,NMDA receptor ,030217 neurology & neurosurgery - Abstract
Excessive glutamate in cerebrospinal fluid after subarachnoid hemorrhage (SAH) causes excitotoxic damage through calcium overloading and a subsequent apoptotic cascade. GluN1/GluN2B containing N-methyl-Daspartate (NMDA) receptor and metabotropic glutamate receptor 1 (mGluR1) can play a leading role in glutamate-mediated excitotoxicity. Here we report that Ifenprodil (100μM), a negative allosteric modulator (NAM) of GluN1/GluN2B NMDA receptors, and JNJ16259685 (10μM), a NAM of mGluR1, have an additive efficacy against glutamate (100μM)-induced Ca2+ release and cell apoptosis in primary cortical, hippocampal, and cerebellar granule neurons. Compared with intraperitoneal injection of Ifenprodil (10mg/kg) and JNJ16259685 (1mg/kg) separately, the combination therapy of Ifenprodil plus JNJ16259685 significantly improves the neurological deficit at 24h and 72h after experimental SAH. It reduces the number of TUNEL/DAPI-positive and activated caspase-3/NeuN-positive cells in cortical and hippocampal CA1 regions at 72h, decreases levels of glutamate in cerebrospinal fluid at 72h, and reduces the mitochondrial Ca2+ concentration. Meanwhile, the combination therapy attenuates apoptosis as shown by an increased Bcl-2 expression, decreased Bax expression and release of cytochrome c, and reduction of cleaved caspase-9 and caspase-3 at 24h after SAH. These findings indicate that targeting both the intracellular Ca2+ overloading and neuronal apoptosis using the Ifenprodil and JNJ16259685 is a promising new therapy for SAH.
- Published
- 2018
19. Harmine enhances GABAergic transmission onto basoamygdala projection neurons in mice
- Author
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Zong-Yong Zhang, Xue-Hui Wang, Xiao-Bin Xu, Wen-Jie You, Bing-Xing Pan, Wei-Zhu Liu, Jun-Yu Zhang, Ping Hu, Wenhua Zhang, and Bo-Wei Huang
- Subjects
Male ,0301 basic medicine ,Patch-Clamp Techniques ,medicine.drug_class ,Postsynaptic Current ,Presynaptic Terminals ,Glutamic Acid ,Inhibitory postsynaptic potential ,Synaptic Transmission ,Anxiolytic ,Amygdala ,Tissue Culture Techniques ,03 medical and health sciences ,Glutamatergic ,chemistry.chemical_compound ,0302 clinical medicine ,Harmine ,Neural Pathways ,medicine ,Animals ,Patch clamp ,gamma-Aminobutyric Acid ,Basolateral Nuclear Complex ,Chemistry ,Pyramidal Cells ,General Neuroscience ,Neural Inhibition ,Mice, Inbred C57BL ,030104 developmental biology ,medicine.anatomical_structure ,Anti-Anxiety Agents ,Excitatory postsynaptic potential ,Neuroscience ,030217 neurology & neurosurgery - Abstract
Emerging evidence indicates that loss of inhibitory tone in amygdala with its subsequent overactivation contributes to the development of multiple mental disorders such as anxiety disorders and post-traumatic stress disorder (PTSD). Harmine is a member of natural β-carboline alkaloids which can readily cross the blood brain barrier and displays significant antidepressant and anxiolytic effects in rodents. However, the underlying neurobiological mechanisms are largely unknown. Here, by using whole-cell patch clamp recordings in in vitro amygdala slices, we examined the effect of harmine on glutamatergic and GABAergic transmission onto basal amygdala (BA) projection neurons (PNs). Our results showed that harmine affected neither the amplitude nor the frequency of spontaneous and miniature excitatory postsynaptic currents (sEPSCs/mEPSCs) of PNs. By contrast, it markedly increased both the amplitude and frequency of the spontaneous inhibitory postsynaptic currents (sIPSCs). For mIPSCs, only an increase of their frequency but not amplitude was observed following harmine perfusion, suggesting that harmine might act through presynaptic mechanism. In parallel, a reduction of paired-pulse ratio of evoked IPSCs emerged in the presence of harmine. Furthermore, the intrinsic excitability of PNs was dramatically decreased upon harmine treatment. Together, our study suggests that harmine selectively potentiates the inhibitory but not excitatory transmission onto BA PNs, which may contribute to its antidepressant and anxiolytic influence.
- Published
- 2018
20. The phosphodiesterase-4 inhibitor roflumilast decreases ethanol consumption in C57BL/6J mice
- Author
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Leilei Mao, Zong-yong Zhang, Bao-liang Sun, Han-Ting Zhang, Ming-feng Yang, Cun-Dong Fan, Xiao-yi Yang, Xin Liu, Pi-da Hao, Jing-yi Sun, and Da-wei Li
- Subjects
Cyclopropanes ,Male ,0301 basic medicine ,Alcohol Drinking ,Aminopyridines ,Alcohol ,Motor Activity ,Pharmacology ,C57bl 6j ,Mice ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Phosphodiesterase 4 Inhibitor ,medicine ,Animals ,PDE4 Inhibitors ,Roflumilast ,Rolipram ,Quinine ,Ethanol ,business.industry ,Cyclic Nucleotide Phosphodiesterases, Type 4 ,Mice, Inbred C57BL ,030104 developmental biology ,chemistry ,Benzamides ,Phosphodiesterase 4 Inhibitors ,business ,030217 neurology & neurosurgery ,medicine.drug - Abstract
Alcohol use disorders have become one of the most damaging psychiatric disorders in the world; however, there are no ideal treatments in clinic. Phosphodiesterase-4 (PDE4), an enzyme that specifically hydrolyzes intracellular cyclic AMP (cAMP), has been involved in alcohol use disorders. Roflumilast is the first PDE4 inhibitor approved for treatment of chronic obstructive pulmonary diseases in clinic. It was of particular interest to researchers to determine whether roflumilast altered ethanol consumption. The present study tried to determine the effects of roflumilast on ethanol intake and preference. We used the two-bottle choice paradigm to assess ethanol intake and preference in C57BL/6J mice treated with roflumilast (1, 3, or 10 mg/kg) or rolipram (0.5 mg/kg; positive control). The effect of roflumilast was verified using the ethanol drinking-in-dark (DID) test. Locomotor activity was examined using the open-field test. Intake of sucrose or quinine was also tested to determine whether natural reward preference and aversive stimuli were involved in the effect of PDE4 inhibitors. Similar to rolipram, roflumilast decreased ethanol intake and preference in two-bottle choice and DID tests in a dose-dependent manner, with significant changes at the dose of 10 mg/kg; in contrast, roflumilast did not affect sucrose or quinine drinking, although it decreased locomotor activity at the high dose within 3 h of treatment. These data provide novel demonstration for the effect of roflumilast on ethanol consumption and suggest that roflumilast may be beneficial for treatment of alcoholism.
- Published
- 2017
21. Adoptive Regulatory T-cell Therapy Attenuates Subarachnoid Hemor-rhage-induced Cerebral Inflammation by Suppressing TLR4/NF-B Signaling Pathway
- Author
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Cun-Dong Fan, Dawei Li, Ming-feng Yang, Lei Zhang, Yuan Wang, Baoliang Sun, Leilei Mao, Zong-yong Zhang, and Liping Zhang
- Subjects
0301 basic medicine ,Adoptive cell transfer ,Subarachnoid hemorrhage ,Regulatory T cell ,Ischemia ,Brain Edema ,Enzyme-Linked Immunosorbent Assay ,Inflammation ,T-Lymphocytes, Regulatory ,Neuroprotection ,03 medical and health sciences ,Cellular and Molecular Neuroscience ,0302 clinical medicine ,Developmental Neuroscience ,medicine ,Animals ,cardiovascular diseases ,business.industry ,Interleukin-2 Receptor alpha Subunit ,NF-kappa B ,Subarachnoid Hemorrhage ,medicine.disease ,Adoptive Transfer ,Rats ,nervous system diseases ,Toll-Like Receptor 4 ,Disease Models, Animal ,030104 developmental biology ,medicine.anatomical_structure ,Matrix Metalloproteinase 9 ,Neurology ,Cerebral blood flow ,Cerebrovascular Circulation ,CD4 Antigens ,Immunology ,TLR4 ,Encephalitis ,medicine.symptom ,business ,030217 neurology & neurosurgery ,Signal Transduction - Abstract
Inflammation is one major cause of poor outcomes of subarachnoid hemorrhage (SAH). The recent evidence suggested that adoptive regulatory T-cell (Treg) therapy conferred potential neuroprotection by suppressing cerebral inflammation against cerebral ischemia. Therefore, we proposed that Treg transfer might protect the brain against SAH by decreasing cerebral inflammation. In this study, we injected the autologous blood into cisterna magna twice to make the SAH model and administrated Tregs by vein to SAH rats. Intriguingly, adoptive transfer of Tregs significantly ameliorated SAH-induced brain edema and increased cerebral blood flow. Moreover, Treg-afforded cerebral protection was accompanied by suppressing SAH-induced cerebral inflammation. Concurrently, administration of Tregs attenuated the activation of the toll-like receptor 4 and nuclear factor-kappa B (TLR4/NF-κB) signaling pathway, which should be involved in the suppression of SAH-induced cerebral inflammation. Altogether, our study suggested that Treg adoptive transfer could attenuate SAH-induced cerebral inflammation by suppressing the activation of the TLR4/NF-κB signaling pathway, and thus provided new insights into the potent Treg cells-based therapy specifically targeting on post-SAH inflammatory dysregulation.
- Published
- 2016
22. DSePA Antagonizes High Glucose-Induced Neurotoxicity: Evidences for DNA Damage-Mediated p53 Phosphorylation and MAPKs and AKT Pathways
- Author
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Ming-feng Yang, Da-wei Li, Hui Yuan, Jing-yi Sun, Xiao-ting Fu, Cun-Dong Fan, Kun Wang, Shuai Zhang, Ya-jun Hou, Zong-yong Zhang, Jie Fang, Bao-liang Sun, Xiao-yi Yang, Leilei Mao, and Xiao-yan Fu
- Subjects
0301 basic medicine ,MAP Kinase Signaling System ,DNA damage ,Poly ADP ribose polymerase ,Neurotoxins ,Neuroscience (miscellaneous) ,Apoptosis ,Mitochondrion ,Biology ,Models, Biological ,PC12 Cells ,03 medical and health sciences ,Cellular and Molecular Neuroscience ,0302 clinical medicine ,medicine ,Animals ,Phosphorylation ,Selenium Compounds ,Protein kinase B ,chemistry.chemical_classification ,Reactive oxygen species ,Neurotoxicity ,medicine.disease ,Mitochondria ,Rats ,Cell biology ,Glucose ,030104 developmental biology ,Proto-Oncogene Proteins c-bcl-2 ,Neurology ,chemistry ,Biochemistry ,Propionates ,Tumor Suppressor Protein p53 ,Reactive Oxygen Species ,Proto-Oncogene Proteins c-akt ,030217 neurology & neurosurgery ,DNA Damage - Abstract
Hyperglycemia as the major hallmark of diabetic neuropathy severely limited its therapeutic efficiency. Evidences have revealed that selenium (Se) as an essential trace element could effectively reduce the risk of neurological diseases. In the present study, 3,3'-diselenodipropionic acid (DSePA), a derivative of selenocystine, was employed to investigate its protective effect against high glucose-induced neurotoxicity in PC12 cells and evaluate the underlying mechanism. The results suggested that high glucose showed significant cytotoxicity through launching mitochondria-mediated apoptosis in PC12 cells, accompanied by poly (ADP-ribose) polymerase (PARP) cleavage, caspase activation, and mitochondrial dysfunction. Moreover, high glucose also triggered DNA damage and dysregulation of MAPKs and AKT pathways through reactive oxygen species (ROS) overproduction. p53 RNA interference partially suppressed high glucose-induced cytotoxicity and apoptosis, indicating the role of p53 in high glucose-induced signal. However, DSePA pretreatment effectively attenuated high glucose-induced cytotoxicity, inhibited the mitochondrial dysfunction through regulation of Bcl-2 family, and ultimately reversed high glucose-induced apoptotic cell death in PC12 cells. Attenuation of caspase activation, PARP cleavage, DNA damage, and ROS accumulation all confirmed its protective effects. Moreover, DSePA markedly alleviated the dysregulation of AKT and MAPKs pathways induced by high glucose. Our findings revealed that the strategy of using DSePA to antagonize high glucose-induced neurotoxicity may be a highly effective strategy in combating high glucose-mediated neurological diseases.
- Published
- 2015
23. Composition, removal, redox, and metal complexation properties of dissolved organic nitrogen in composting leachates
- Author
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Xiao-Song He, Zong-Yong Zhang, Beidou Xi, Ying Yuan, Wenbing Tan, Ru-Tai Gao, and Dongyu Cui
- Subjects
Environmental Engineering ,Nitrogen ,Health, Toxicology and Mutagenesis ,Inorganic chemistry ,Redox ,Metal ,Soil ,Coordination Complexes ,Dissolved organic carbon ,Environmental Chemistry ,Leachate ,Waste Management and Disposal ,Effluent ,Humic Substances ,chemistry.chemical_classification ,Chemistry ,Pollution ,Refuse Disposal ,Amino acid ,Environmental chemistry ,visual_art ,visual_art.visual_art_medium ,Composition (visual arts) ,Oxidation-Reduction ,Water Pollutants, Chemical ,Dissolved organic nitrogen ,Environmental Monitoring - Abstract
This study investigated the composition, removal, redox, and metal complexation characteristics of dissolved organic nitrogen (DON) in composting leachates. Results showed that the leachate-derived DON comprised proteinaceous compounds and amines, and most of them were integrated into the fulvic- and humic-like substances. Neutral, basic, acidic, hydroxylic, aromatic, and sulfuric amino acids all were detected in the influent leachates. However, most of them were removed by the biological and physical processes, and only neutral amino acids were detected in the effluent. The DON was not the main contributor to the redox capability of the leachate dissolved organic matter (DOM). However, it exhibited a strong capability for metal complexation. The amines formed strong complexes with the metals Mo, Co, Cr, and Ni, while the proteinaceous matter interacted with the metals Cr and Ni.
- Published
- 2015
24. Cysteamine Alleviates Early Brain Injury Via Reducing Oxidative Stress and Apoptosis in a Rat Experimental Subarachnoid Hemorrhage Model
- Author
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Bao-liang Sun, Zong-yong Zhang, Yun-lin Liu, Da-wei Li, Tao Wang, Ming-feng Yang, and Jin-hui Zhang
- Subjects
Male ,Subarachnoid hemorrhage ,Cysteamine ,Fluorescent Antibody Technique ,Apoptosis ,Brain Edema ,Pharmacology ,medicine.disease_cause ,Neuroprotection ,Permeability ,Rats, Sprague-Dawley ,Cellular and Molecular Neuroscience ,chemistry.chemical_compound ,In Situ Nick-End Labeling ,medicine ,Animals ,cardiovascular diseases ,Cerebral Cortex ,chemistry.chemical_classification ,Reactive oxygen species ,Behavior, Animal ,Caspase 3 ,business.industry ,Brain-Derived Neurotrophic Factor ,Glutathione peroxidase ,Cell Biology ,General Medicine ,Glutathione ,Subarachnoid Hemorrhage ,Malondialdehyde ,medicine.disease ,nervous system diseases ,Disease Models, Animal ,Oxidative Stress ,chemistry ,Blood-Brain Barrier ,Brain Injuries ,Anesthesia ,Reactive Oxygen Species ,business ,Oxidative stress - Abstract
Oxidative stress plays an important role in the pathogenesis of early brain injury (EBI) following subarachnoid hemorrhage (SAH). The aim of this study was to assess whether cysteamine prevents post-SAH oxidative stress injury via its antioxidative and anti-apoptotic effects. It was observed that intraperitoneal administration of cysteamine (20 mg/kg/day) could significantly alleviate EBI (including neurobehavioral deficits, brain edema, blood-brain barrier permeability, and cortical neuron apoptosis) after SAH in rats. Meanwhile, cysteamine treatment reduced post-SAH elevated the reactive oxygen species level, the concentration of malondialdehyde, 3-nitrotyrosine, and 8-hydroxydeoxyguanosine and increased the glutathione peroxidase enzymatic activity, the concentration of glutathione and brain-derived neurotrophic factor in brain cortex at 48 h after SAH. These results indicated that administration of cysteamine may ameliorate EBI and provide neuroprotection after SAH in rat models.
- Published
- 2014
25. Intranasal Delivery of Granulocyte Colony-Stimulating Factor Enhances Its Neuroprotective Effects Against Ischemic Brain Injury in Rats
- Author
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Cun-Dong Fan, Shuai Zhang, Da-wei Li, Xiang-yu Han, Feng Zhang, Jing-yi Sun, Ming-feng Yang, Zong-yong Zhang, R. Anne Stetler, Bao-liang Sun, Cheng-Bi Zheng, Xiao-yi Yang, Yang V. Li, Hui Yuan, Leilei Mao, Mei-qing He, and Jun Chen
- Subjects
Brain Infarction ,Male ,0301 basic medicine ,Neurogenesis ,Hematopoietic growth factor ,Central nervous system ,Intracellular Space ,Neuroscience (miscellaneous) ,Ischemia ,Neovascularization, Physiologic ,Pharmacology ,Neuroprotection ,Brain Ischemia ,Rats, Sprague-Dawley ,Brain ischemia ,03 medical and health sciences ,Cellular and Molecular Neuroscience ,0302 clinical medicine ,Cerebrospinal fluid ,Tubulin ,Granulocyte Colony-Stimulating Factor ,Animals ,Medicine ,Administration, Intranasal ,Cytoskeleton ,business.industry ,Brain ,Infarction, Middle Cerebral Artery ,medicine.disease ,Up-Regulation ,Granulocyte colony-stimulating factor ,Neuroprotective Agents ,030104 developmental biology ,medicine.anatomical_structure ,Neurology ,Anesthesia ,Calcium ,Nasal administration ,business ,Heme Oxygenase-1 ,030217 neurology & neurosurgery - Abstract
Granulocyte colony-stimulating factor (G-CSF) is a hematopoietic growth factor with strong neuroprotective properties. However, it has limited capacity to cross the blood-brain barrier and thus potentially limiting its protective capacity. Recent studies demonstrated that intranasal drug administration is a promising way in delivering neuroprotective agents to the central nervous system. The current study therefore aimed at determining whether intranasal administration of G-CSF increases its delivery to the brain and its neuroprotective effect against ischemic brain injury. Transient focal cerebral ischemia in rat was induced with middle cerebral artery occlusion. Our resulted showed that intranasal administration is 8-12 times more effective than subcutaneous injection in delivering G-CSF to cerebrospinal fluid and brain parenchyma. Intranasal delivery enhanced the protective effects of G-CSF against ischemic injury in rats, indicated by decreased infarct volume and increased recovery of neurological function. The neuroprotective mechanisms of G-CSF involved enhanced upregulation of HO-1 and reduced calcium overload following ischemia. Intranasal G-CSF application also promoted angiogenesis and neurogenesis following brain ischemia. Taken together, G-CSF is a legitimate neuroprotective agent and intranasal administration of G-CSF is more effective in delivery and neuroprotection and could be a practical approach in clinic.
- Published
- 2014
26. Roflumilast Reduces Cerebral Inflammation in a Rat Model of Experimental Subarachnoid Hemorrhage
- Author
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Xiao-yi Yang, Lifeng Qi, Rongxia Xie, Qingjian Wu, Zong-yong Zhang, Leilei Mao, Jian Wang, Jiming Kong, Mingfeng Yang, Hanxia Li, and Baoliang Sun
- Subjects
Cyclopropanes ,0301 basic medicine ,medicine.medical_specialty ,Subarachnoid hemorrhage ,Immunology ,Rat model ,Aminopyridines ,Apoptosis ,Brain Edema ,Inflammation ,Pharmacology ,Permeability ,Article ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Internal medicine ,medicine ,Animals ,Immunology and Allergy ,Roflumilast ,Evans Blue ,COPD ,business.industry ,Brain ,Subarachnoid Hemorrhage ,medicine.disease ,Rheumatology ,Extravasation ,Rats ,030104 developmental biology ,chemistry ,Blood-Brain Barrier ,Anesthesia ,Benzamides ,Phosphodiesterase 4 Inhibitors ,Inflammation Mediators ,medicine.symptom ,business ,030217 neurology & neurosurgery ,medicine.drug - Abstract
Roflumilast, a selective inhibitor for PDE4, is approved by FDA as an anti-inflammation drug for treatment of chronic obstructive pulmonary disease (COPD). This study investigates the effects of roflumilast on cerebral inflammation in the rat SAH model. Here, we show that subcutaneous administration of roflumilast (3 mg/kg) significantly improved the neurological deficits. Measurement of evans blue extravasation and brain water content revealed a significant reduction of blood-brain barrier permeability and brain edema. Importantly, roflumilast treatment remarkably decreased levels of IL-1β, IL-6, and TNF-α and the number of apoptotic neurons in the brain after SAH. These results indicate that roflumilast is effective in treating cerebral inflammation following SAH.
- Published
- 2017
27. Author response: Allosteric control of an asymmetric transduction in a G protein-coupled receptor heterodimer
- Author
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Ana Trapero, James A. R. Dalton, Xavier Rovira, Siluo Huang, Jianfeng Liu, Cyril Goudet, Jesús Giraldo, Junke Liu, Zong-yong Zhang, Amadeu Llebaria, Philippe Rondard, David Moreno-Delgado, Jean-Philippe Pin, and Qilin Yuan
- Subjects
Transduction (genetics) ,Chemistry ,G-protein coupled receptor heterodimer ,Allosteric regulation ,Cell biology - Published
- 2017
28. The effect of mental countermeasures on fMRI-based concealed information tests
- Author
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Da-Wei Li, Arunkumar Prasad, Lei-Lei Mao, Li Jia, Cun-Dong Fan, Yang, Zi-Cui Cheng, Xi-chang Liu, Bao-liang Sun, Ming-Feng Yang, Li-Li Jia, Zong-yong Zhang, Xuan Wang, Cheng-Bi Zhengb, and Xiao-Yi
- Subjects
Cerebral injury ,Subarachnoid hemorrhage ,biology ,business.industry ,Ginkgo biloba ,Ginkgo ,Vasospasm ,medicine.disease ,biology.organism_classification ,Blockade ,Cerebral vasospasm ,Lymphatic system ,Anesthesia ,medicine ,business - Published
- 2017
29. Adoptive Regulatory T-cell Therapy Attenuates Perihematomal Inflammation in a Mouse Model of Experimental Intracerebral Hemorrhage
- Author
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Leilei Mao, Wen-wen Wang, Zong-yong Zhang, Bao-liang Sun, Ming-feng Yang, Xiao-yi Yang, Yu-jing Wang, and Hui Yuan
- Subjects
0301 basic medicine ,Male ,Adoptive cell transfer ,Regulatory T cell ,Inflammation ,Apoptosis ,T-Lymphocytes, Regulatory ,Proinflammatory cytokine ,03 medical and health sciences ,Cellular and Molecular Neuroscience ,0302 clinical medicine ,Malondialdehyde ,medicine ,Animals ,cardiovascular diseases ,IL-2 receptor ,Cerebral Hemorrhage ,Hematoma ,business.industry ,Superoxide Dismutase ,Transcription Factor RelA ,Interleukin ,Cell Biology ,General Medicine ,Adoptive Transfer ,Extravasation ,Mice, Inbred C57BL ,Disease Models, Animal ,030104 developmental biology ,medicine.anatomical_structure ,Blood-Brain Barrier ,Immunology ,Cytokines ,Tumor necrosis factor alpha ,medicine.symptom ,business ,030217 neurology & neurosurgery - Abstract
The CD4+CD25+ regulatory T cells (Tregs), an innate immunomodulator, suppress cerebral inflammation and maintain immune homeostasis in multiple central nervous system injury, but its role in intracerebral hemorrhage (ICH) has not been fully characterized. This study investigated the effect of Tregs on brain injury using the mouse ICH model, which is established by autologous blood infusion. The results showed that tail intravenous injection of Tregs significantly reduced brain water content and Evans blue dye extravasation of perihematoma at day (1, 3 and 7), and improved short- and long-term neurological deficits following ICH in mouse model. Tregs treatment reduced the content of pro-inflammatory cytokines interleukin (IL)-1β, IL-6, tumor necrosis factor-α, and malondialdehyde, while increasing the superoxide dismutase (SOD) enzymatic activity at day (1, 3 and 7) following ICH. Furthermore, Tregs treatment obviously reduced the number of NF-κB+, IL-6+, TUNEL+ and active caspase-3+ cells at day 3 after ICH. These results indicate that adoptive transfer of Tregs may provide neuroprotection following ICH in mouse models.
- Published
- 2016
30. Carnosine Attenuates Brain Oxidative Stress and Apoptosis After Intracerebral Hemorrhage in Rats
- Author
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Rongxia Xie, Xi-chang Liu, Bao-liang Sun, Ming-feng Yang, Zong-yong Zhang, Jie Fang, Xiao-yi Yang, and Da-wei Li
- Subjects
0301 basic medicine ,Male ,Carnosine ,Apoptosis ,Pharmacology ,Blood–brain barrier ,medicine.disease_cause ,Occludin ,Biochemistry ,Neuroprotection ,Rats, Sprague-Dawley ,03 medical and health sciences ,Cellular and Molecular Neuroscience ,chemistry.chemical_compound ,Random Allocation ,0302 clinical medicine ,medicine ,Animals ,Cerebral Hemorrhage ,TUNEL assay ,Microglia ,Chemistry ,Brain ,General Medicine ,Rats ,Oxidative Stress ,030104 developmental biology ,medicine.anatomical_structure ,030217 neurology & neurosurgery ,Oxidative stress - Abstract
Carnosine, an endogenous dipeptide (β-alanyl-l-histidine), exerts multiple neuroprotective properties, but its role in intracerebral hemorrhage (ICH) remains unclear. This study investigates the effect of Carnosine on brain injury using the rat ICH model, which is established by type IV collagenase caudatum infusion. The results indicate that intraperitoneal administration of Carnosine (1000 mg/kg) significantly attenuates brain edema, blood–brain barrier (BBB) disruption, oxidative stress, microglia activation and neuronal apoptosis of perihematoma at 72 h following ICH in rats models, as convinced by preventing the disruption of tight junction protein ZO-1, occludin and claudin-5, followed by the decrease of ROS, MDA, 3-NT, 8-OHDG level and the increase of GSH-Px and SOD activity, then followed by the decline of Iba-1, ED-1, active caspase-3 and TUNEL positive cells and the decrease of IL-1β, IL-6, TNF-α, active caspase-3 and cytochrome c level. Our results suggest that Carnosine may provide neuroprotective effect after experimental ICH in rat models.
- Published
- 2016
31. Is CO
- Author
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Yu, Hao, Zong-Yong, Zhang, Hua, Liao, Yi-Ming, Wei, and Shuo, Wang
- Subjects
Air Pollutants ,China ,Economic Development ,Carbon Dioxide ,Environment - Abstract
Based on panel data for 29 Chinese provinces from 1995 to 2012, this paper explores the relationship between financial development and environmental quality in China. A comprehensive framework is utilized to estimate both the direct and indirect effects of financial development on CO
- Published
- 2016
32. Enhanced Therapeutic Potential of Nano-Curcumin Against Subarachnoid Hemorrhage-Induced Blood-Brain Barrier Disruption Through Inhibition of Inflammatory Response and Oxidative Stress
- Author
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Xiao-yan Fu, Cun-Dong Fan, Ming-feng Yang, Yan-Xin Yin, Jie Fang, Shuai Zhang, Leilei Mao, Bao-liang Sun, Da-wei Li, Xiao-ting Fu, Ming Jiang, Zong-yong Zhang, and Ya-jun Hou
- Subjects
0301 basic medicine ,Male ,Curcumin ,Perforation (oil well) ,Neuroscience (miscellaneous) ,Pharmacology ,Occludin ,Blood–brain barrier ,medicine.disease_cause ,Neuroprotection ,Rats, Sprague-Dawley ,03 medical and health sciences ,Cellular and Molecular Neuroscience ,chemistry.chemical_compound ,Random Allocation ,0302 clinical medicine ,Polylactic Acid-Polyglycolic Acid Copolymer ,Medicine ,Animals ,cardiovascular diseases ,Lactic Acid ,Mortality ,Evans Blue ,Dose-Response Relationship, Drug ,business.industry ,technology, industry, and agriculture ,Subarachnoid Hemorrhage ,Extravasation ,nervous system diseases ,Rats ,Oxidative Stress ,030104 developmental biology ,medicine.anatomical_structure ,Neuroprotective Agents ,Neurology ,chemistry ,Blood-Brain Barrier ,Anesthesia ,Nanoparticles ,Inflammation Mediators ,business ,030217 neurology & neurosurgery ,Oxidative stress ,Polyglycolic Acid - Abstract
Curcumin and nano-curcumin both exhibit neuroprotective effects in early brain injury (EBI) after experimental subarachnoid hemorrhage (SAH). However, the mechanism that whether curcumin and its nanoparticles affect the blood-brain barrier (BBB) following SAH remains unclear. This study investigated the effect of curcumin and the poly(lactide-co-glycolide) (PLGA)-encapsulated curcumin nanoparticles (Cur-NPs) on BBB disruption and evaluated the possible mechanism underlying BBB dysfunction in EBI using the endovascular perforation rat SAH model. The results indicated that Cur-NPs showed enhanced therapeutic effects than that of curcumin in improving neurological function, reducing brain water content, and Evans blue dye extravasation after SAH. Mechanically, Cur-NPs attenuated BBB dysfunction after SAH by preventing the disruption of tight junction protein (ZO-1, occludin, and claudin-5). Cur-NPs also up-regulated glutamate transporter-1 and attenuated glutamate concentration of cerebrospinal fluid following SAH. Moreover, inhibition of inflammatory response and microglia activation both contributed to Cur-NPs' protective effects. Additionally, Cur-NPs markedly suppressed SAH-mediated oxidative stress and eventually reversed SAH-induced cell apoptosis in rats. Our findings revealed that the strategy of using Cur-NPs could be a promising way in improving neurological function in EBI after experimental rat SAH.
- Published
- 2015
33. Enhanced Neuroprotection of Minimally Invasive Surgery Joint Local Cooling Lavage against ICH-induced Inflammation Injury and Apoptosis in Rats
- Author
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Xiao-yan Fu, Yuan Wang, Ming-feng Yang, Jing-yi Sun, Xi-chang Liu, Zong-yong Zhang, Ya-jun Hou, Leilei Mao, Li-yan Jing, Cun-dong Fan, You-mei Tang, Kun Wang, Jie Fang, Da-wei Li, Bao-liang Sun, Xiao-yi Yang, and Xiao-ting Fu
- Subjects
0301 basic medicine ,Male ,medicine.medical_treatment ,Inflammation ,Apoptosis ,Brain Edema ,Brain damage ,Neuroprotection ,Rats, Sprague-Dawley ,03 medical and health sciences ,Cellular and Molecular Neuroscience ,0302 clinical medicine ,Hematoma ,otorhinolaryngologic diseases ,medicine ,Animals ,Minimally Invasive Surgical Procedures ,cardiovascular diseases ,Therapeutic Irrigation ,Saline ,Cerebral Hemorrhage ,Intracerebral hemorrhage ,Neurons ,business.industry ,Therapeutic effect ,Cell Biology ,General Medicine ,Recovery of Function ,medicine.disease ,030104 developmental biology ,Anesthesia ,Brain Injuries ,medicine.symptom ,business ,030217 neurology & neurosurgery - Abstract
Hypothermia treatment is one of the neuroprotective strategies that improve neurological outcomes effectively after brain damage. Minimally invasive surgery (MIS) has been an important treatment of intracerebral hemorrhage (ICH). Herein, we evaluated the neuroprotective effect and mechanism of MIS joint local cooling lavage (LCL) treatment on ICH via detecting the inflammatory responses, oxidative injury, and neuronal apoptosis around the hematoma cavity in rats. ICH model was established by type IV collagenase caudatum infusion. The rats were treated with MIS 6 h after injection, and then were lavaged by normothermic (37 °C) and hypothermic (33 °C) normal saline in brain separately. The results indicated that MIS joint LCL treatment showed enhanced therapeutic effects against ICH-induced inflammation injury and apoptosis in rats, as convinced by the decline of TUNEL-positive cells, followed by the decrease of IL-1β and LDH and increase of IL-10 and SOD. This study demonstrated that the strategy of using MIS joint LCL may achieve enhanced neuroprotection against ICH-induced inflammation injury and apoptosis in rats with potential clinic application.
- Published
- 2015
34. Inhibition of phosphodiesterase‐4 (PDE4) by roflumilast decreases ethanol consumption
- Author
-
Ming-feng Yang, Zong-yong Zhang, Bao-liang Sun, Xin Liu, Pi-da Hao, Han-Ting Zhang, and Da-wei Li
- Subjects
Consumption (economics) ,chemistry.chemical_compound ,Phosphodiesterase-4 ,Ethanol ,chemistry ,Genetics ,medicine ,Pharmacology ,Molecular Biology ,Biochemistry ,Roflumilast ,Biotechnology ,medicine.drug - Published
- 2015
35. Activation of mGluR5 Attenuates Microglial Activation and Neuronal Apoptosis in Early Brain Injury After Experimental Subarachnoid Hemorrhage in Rats
- Author
-
Shuai Zhang, Jie Fang, Ming-feng Yang, Da-wei Li, Zong-yong Zhang, Bao-liang Sun, Qilin Yuan, Siluo Huang, and Junke Liu
- Subjects
Agonist ,Male ,Allosteric modulator ,Subarachnoid hemorrhage ,medicine.drug_class ,Receptor, Metabotropic Glutamate 5 ,Central nervous system ,Glycine ,Apoptosis ,Brain Edema ,Pharmacology ,Biochemistry ,Neuroprotection ,Rats, Sprague-Dawley ,Cellular and Molecular Neuroscience ,mental disorders ,medicine ,Excitatory Amino Acid Agonists ,Animals ,Cyclin D1 ,cardiovascular diseases ,Receptor ,Phenylacetates ,bcl-2-Associated X Protein ,Cerebral Cortex ,Neurons ,Microglia ,Behavior, Animal ,business.industry ,Metabotropic glutamate receptor 5 ,Caspase 3 ,General Medicine ,Macrophage Activation ,Subarachnoid Hemorrhage ,medicine.disease ,nervous system diseases ,Rats ,medicine.anatomical_structure ,nervous system ,Cytokines ,business ,Neuroscience - Abstract
Activation of metabotropic glutamate receptor 5 (mGluR5) provided neuroprotection in multiple central nervous system injury, but the roles of mGluR5 in subarachnoid hemorrhage (SAH) remain unclear. In present study, we aimed to evaluate whether activation of mGluR5 attenuates early brain injury (EBI) after experimental SAH in rats. We found that selective mGluR5 orthosteric agonist CHPG or positive allosteric modulator VU0360172 administration significantly improves neurological function and attenuates brain edema at 24 h after SAH. Furthermore, mGluR5 obviously expresses in activated microglia (ED-1 positive) after SAH. CHPG or VU0360172 administration significantly reduces the numbers of activated microglia and the protein and mRNA levels of pro-inflammatory cytokines IL-1β, IL-6 and TNF-α at 24 h after SAH. Moreover, CHPG or VU0360172 administration obviously reduces the number of TUNEL-positive cells and active caspase-3/NeuN-positive neurons in cortex at 24 h after SAH. CHPG or VU0360172 administration significantly up-regulates the expression of Bcl-2, and down-regulates the expression of Bax and active caspase-3, which in turn increases the ratio of Bcl-2/Bax. Our results indicate that activation of mGluR5 attenuates microglial activation and neuronal apoptosis, and improves neurological function in EBI after SAH.
- Published
- 2015
36. Attenuation of Cisplatin-Induced Neurotoxicity by Cyanidin, a Natural Inhibitor of ROS-Mediated Apoptosis in PC12 Cells
- Author
-
Cun-dong Fan, Shuai Zhang, Bao-liang Sun, Jie Fang, Hui Yuan, Da-wei Li, Mei-jia Zhu, Jing-yi Sun, Zong-yong Zhang, Kun Wang, Xiao-yan Fu, Ya-jun Hou, Leilei Mao, and Ming-feng Yang
- Subjects
Antioxidant ,DNA damage ,Cell Survival ,medicine.medical_treatment ,Cyanidin ,Apoptosis ,Pharmacology ,PC12 Cells ,Anthocyanins ,Cellular and Molecular Neuroscience ,chemistry.chemical_compound ,medicine ,Animals ,Cytotoxicity ,chemistry.chemical_classification ,Cisplatin ,Reactive oxygen species ,Dose-Response Relationship, Drug ,Neurotoxicity ,food and beverages ,Cell Biology ,General Medicine ,medicine.disease ,Rats ,Oxidative Stress ,chemistry ,Biochemistry ,Reactive Oxygen Species ,medicine.drug - Abstract
Cisplatin-based chemotherapy in clinic is severely limited by its adverse effect, including neurotoxicity. Oxidative damage contributes to cisplatin-induced neurotoxicity, but the mechanism remains unclearly. Cyanidin, a natural flavonoid compound, exhibits powerful antioxidant activity. Hence, we investigated the protective effects of cyanidin on PC12 cells against cisplatin-induced neurotoxicity and explored the underlying mechanisms. The results showed that cisplatin-induced cytotoxicity was completely reversed by cyanidin through inhibition of PC12 cell apoptosis, as proved by the attenuation of Sub-G1 peak, PARP cleavage, and caspases-3 activation. Mechanistically, cyanidin significantly inhibited reactive oxygen species (ROS)-induced DNA damage in cisplatin-treated PC12 cells. Our findings revealed that cyanidin as an apoptotic inhibitor effectively blocked cisplatin-induced neurotoxicity through inhibition of ROS-mediated DNA damage and apoptosis, predicating its therapeutic potential in prevention of chemotherapy-induced neurotoxicity. Cisplatin caused DNA damage, activated p53, and subsequently induced PC12 cells apoptosis by triggering ROS overproduction. However, cyanidin administration effectively inhibited DNA damage, attenuated p53 phosphorylation, and eventually reversed cisplatin-induced PC12 cell apoptosis through inhibition ROS accumulation.
- Published
- 2014
37. GABAB receptor promotes its own surface expression by recruiting a Rap1-dependent signaling cascade
- Author
-
Yunyun Wang, Zong-yong Zhang, Jean-Philippe Pin, Siluo Huang, Zhihua Jiang, Nagahiro Minato, Jianfeng Liu, Qian Sun, Li Su, Yilei Zhang, Yongjian Hu, Wenhua Zhang, and Ninghua Sun
- Subjects
Receptor recycling ,Male ,B-cell receptor ,Blotting, Western ,Molecular Sequence Data ,Fluorescent Antibody Technique ,Biology ,δ-opioid receptor ,Mice ,GABA receptor ,Neurotransmitter receptor ,Enzyme-linked receptor ,Animals ,5-HT5A receptor ,Biotinylation ,Amino Acid Sequence ,Phosphorylation ,Cells, Cultured ,Neurons ,Sequence Homology, Amino Acid ,Cell Membrane ,rap1 GTP-Binding Proteins ,Cell Biology ,Flow Cytometry ,Endocytosis ,Cell biology ,nervous system ,Receptors, GABA-B ,Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ,Estrogen-related receptor gamma ,Female ,Signal Transduction - Abstract
G-protein-coupled receptors (GPCRs) are key players in cell signaling, and their cell surface expression is tightly regulated. For many GPCRs such as β2-AR (β2-adrenergic receptor), receptor activation leads to downregulation of receptor surface expression, a phenomenon that has been extensively characterized. By contrast, some other GPCRs, such as GABAB receptor, remain relatively stable at the cell surface even after prolonged agonist treatment; however, the underlying mechanisms are unclear. Here, we identify the small GTPase Rap1 as a key regulator for promoting GABAB receptor surface expression. Agonist stimulation of GABAB receptor signals through Gαi/o to inhibit Rap1GAPII (also known as Rap1GAP1b, an isoform of Rap1GAP1), thereby activating Rap1 (which has two isoforms, Rap1a and Rap1b) in cultured cerebellar granule neurons (CGNs). The active form of Rap1 is then recruited to GABAB receptor through physical interactions in CGNs. This Rap1-dependent signaling cascade promotes GABAB receptor surface expression by stimulating receptor recycling. Our results uncover a new mechanism regulating GPCR surface expression and also provide a potential explanation for the slow, long-lasting inhibitory action of GABA neurotransmitter.
- Published
- 2014
38. Strategy to Suppress Oxidative Damage-Induced Neurotoxicity in PC12 Cells by Curcumin: the Role of ROS-Mediated DNA Damage and the MAPK and AKT Pathways
- Author
-
Zong-yong Zhang, Ming-zhi Cao, Da-wei Li, Feng-ze Wang, Cun-Dong Fan, Bao-liang Sun, Leilei Mao, Xiao-yan Fu, Shuai Zhang, Ming-feng Yang, Feng Zhang, Xiao-yi Yang, and Jing-yi Sun
- Subjects
0301 basic medicine ,MAPK/ERK pathway ,Curcumin ,DNA damage ,MAP Kinase Signaling System ,Poly ADP ribose polymerase ,Neurotoxins ,Neuroscience (miscellaneous) ,Apoptosis ,Biology ,medicine.disease_cause ,Models, Biological ,PC12 Cells ,03 medical and health sciences ,Cellular and Molecular Neuroscience ,chemistry.chemical_compound ,0302 clinical medicine ,medicine ,Animals ,Protein kinase B ,chemistry.chemical_classification ,Membrane Potential, Mitochondrial ,Reactive oxygen species ,Neurotoxicity ,Hydrogen Peroxide ,medicine.disease ,Cell biology ,Rats ,Oxidative Stress ,030104 developmental biology ,Neuroprotective Agents ,Neurology ,chemistry ,Proto-Oncogene Proteins c-bcl-2 ,Reactive Oxygen Species ,Proto-Oncogene Proteins c-akt ,030217 neurology & neurosurgery ,Oxidative stress ,DNA Damage - Abstract
Oxidative damage plays a key role in causation and progression of neurodegenerative diseases. Inhibition of oxidative stress represents one of the most effective ways in treating human neurologic diseases. Herein, we evaluated the protective effect of curcumin on PC12 cells against H2O2-induced neurotoxicity and investigated its underlying mechanism. The results indicated that curcumin pre-treatment significantly suppressed H2O2-induced cytotoxicity, inhibited the loss of mitochondrial membrane potential (Δψm) through regulation of Bcl-2 family expression, and ultimately reversed H2O2-induced apoptotic cell death in PC12 cells. Attenuation of caspase activation, poly(ADP-ribose) polymerase (PARP) cleavage, DNA damage, and accumulation of reactive oxygen species (ROS) all confirmed its protective effects. Moreover, curcumin markedly alleviated the dysregulation of the MAPK and AKT pathways induced by H2O2. Taken together, our findings suggest that the strategy of using curcumin could be a highly effective way in combating oxidative damage-mediated human neurodegenerative diseases.
- Published
- 2014
39. China's Farewell to Coal: A Forecast of Coal Consumption through 2020
- Author
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Yu Hao, Zong-Yong Zhang, Hua Liao, and Yi-Ming Wei
- Subjects
Coal consumption, Environmental Kuznets Curve, Spatial correlation, Panel data, Forecast ,jel:Q47 ,complex mixtures - Abstract
In recent decades, China has encountered serious environmental problem, especially severe air pollution that has affected eastern and northern China frequently. Because most air pollutants in China are closely related to coal combustion, the restriction of coal consumption is critical to the improvement of the environment in China. In this study, a panel of 29 Chinese provinces from 1995 to 2012 is utilized to predict China's coal consumption through 2020. After controlling for the spatial correlation of coal consumption among neighboring provinces, an inverted U-shaped Environmental Kuznets Curve (EKC) between coal consumption per capita and GDP per capita in China is detected. Furthermore, based on the estimation results and reasonable predictions of key control variables, China's provincial and national coal consumption through 2020 is forecasted. Specifically, under the benchmark scenario, consumption is expected to continue growing at a decreasing rate until 2020, when China's coal consumption would be approximately 4.43 billion tons. However, if China can maintain relatively high growth rate (an annual growth rate of 7.8 percent), the turning point in total coal consumption would occur in 2019, with projected consumption peaking at 4.16 billion tons.
- Published
- 2014
40. Carnosine attenuates early brain injury through its antioxidative and anti-apoptotic effects in a rat experimental subarachnoid hemorrhage model
- Author
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Da-wei Li, Zong-yong Zhang, Shuai Zhang, Jie Fang, Bao-liang Sun, and Ming-feng Yang
- Subjects
Male ,Carnosine ,Fluorescent Antibody Technique ,Apoptosis ,Brain Edema ,Nerve Tissue Proteins ,Pharmacology ,Neuroprotection ,Antioxidants ,Permeability ,Superoxide dismutase ,Rats, Sprague-Dawley ,Cellular and Molecular Neuroscience ,chemistry.chemical_compound ,medicine ,In Situ Nick-End Labeling ,Animals ,chemistry.chemical_classification ,Cerebral Cortex ,Reactive oxygen species ,Glutathione Peroxidase ,Microglia ,biology ,Behavior, Animal ,Caspase 3 ,Superoxide Dismutase ,Glutathione peroxidase ,Interleukin ,Antigens, Nuclear ,Cell Biology ,General Medicine ,DNA ,Subarachnoid Hemorrhage ,Malondialdehyde ,Lipids ,Disease Models, Animal ,medicine.anatomical_structure ,chemistry ,Blood-Brain Barrier ,Anesthesia ,Brain Injuries ,biology.protein ,Cytokines ,Reactive Oxygen Species ,Oxidation-Reduction - Abstract
Carnosine (β-alanyl-l-histidine) has been demonstrated to provide antioxidative and anti-apoptotic roles in the animal of ischemic brain injuries and neurodegenerative diseases. The aim of this study was to examine whether carnosine prevents subarachnoid hemorrhage (SAH)-induced early brain injury (EBI) in rats. We found that intraperitoneal administration of carnosine improved neurobehavioral deficits, attenuated brain edema and blood–brain barrier permeability, and decreased reactive oxygen species level at 48 h following SAH in rat models. Carnosine treatment increased tissue copper/zinc superoxide dismutase (CuZn-SOD) and glutathione peroxidase (GSH-Px) enzymatic activities, and reduced post-SAH elevated lactate dehydrogenase (LDH) activity, the concentration of malondialdehyde (MDA), 3-nitrotyrosine (3-NT), 8-hydroxydeoxyguanosine (8-OHDG), interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α) in rats. Furthermore, carnosine treatment attenuated SAH-induced microglia activation and cortical neuron apoptosis. These results indicated that administration of carnosine may provide neuroprotection in EBI following SAH in rat models.
- Published
- 2014
41. Insight into the evolution, redox, and metal binding properties of dissolved organic matter from municipal solid wastes using two-dimensional correlation spectroscopy
- Author
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Wen-Bing Tan, Xiao-Song He, Beidou Xi, Dong-Yu Cui, Ru-Tai Gao, and Zong-Yong Zhang
- Subjects
Environmental Engineering ,Health, Toxicology and Mutagenesis ,Inorganic chemistry ,Solid Waste ,Redox ,chemistry.chemical_compound ,Dissolved organic carbon ,Environmental Chemistry ,Lignin ,Hemicellulose ,Recycling ,Cellulose ,Organic Chemicals ,Humic Substances ,Chemistry ,Metal binding ,Spectrum Analysis ,Public Health, Environmental and Occupational Health ,General Medicine ,General Chemistry ,Pollution ,Refuse Disposal ,Zn binding ,Metals ,Two-dimensional nuclear magnetic resonance spectroscopy ,Oxidation-Reduction - Abstract
Two-dimensional correlation spectroscopy was employed to investigate the evolution, redox, and metal binding properties of dissolved organic matter (DOM) from municipal solid wastes (MSWs) during composting. The results showed that the DOM was degraded during composting in the order of aliphatic substances > proteinaceous compounds > cellulose, hemicellulose and lignin, while humic substances transformed during the process in the order of fulvic-like matter > humic-like substances > protein-like matter. The fulvic- and humic-like substances originated from lignin and polysaccharide-like substances with the function groups of CH3, CCH2, CCH, OCH3, OCH, O--C--O, aromatic C, and COO, while the protein-like matter was derived from aliphatic and proteinaceous compounds with the functional groups of CCH3 and N--C==O. The aromatic C and COO were responsible for the oxidation capacity of the MSW-derived DOM, while the O--C--O and COO accounted for the Cu and Zn binding capacity of the DOM.
- Published
- 2014
42. High SIPA-1 expression in proximal tubules of human kidneys under pathological conditions
- Author
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Shao-zhong Wei, Zong-yong Zhang, Xinnong Jiang, Li Su, Aiping Feng, Peng Zhu, Min Li, Qian Zhang, and Ming-wei Wang
- Subjects
Pathology ,medicine.medical_specialty ,Biomedical Engineering ,Apoptosis ,Biology ,Biochemistry ,Cell Line ,Biomaterials ,Pathogenesis ,Kidney Tubules, Proximal ,Renal cell carcinoma ,Genetics ,medicine ,Carcinoma ,Humans ,Lupus Erythematosus, Systemic ,Earth-Surface Processes ,Cell Proliferation ,DNA Primers ,Autoimmune disease ,Kidney ,Lupus erythematosus ,Base Sequence ,Cell growth ,Reverse Transcriptase Polymerase Chain Reaction ,GTPase-Activating Proteins ,Nuclear Proteins ,medicine.disease ,Clear cell renal cell carcinoma ,medicine.anatomical_structure - Abstract
Systemic lupus erythematosus (SLE) and clear cell renal cell carcinoma (CC-RCC) are serious disorders and usually fatal, and always accompanied with pathological changes in the kidney. Signal-induced proliferation-associated protein 1 (SIPA-1) is a Rap1GTPase activating protein (Rap1GAP) expressed in the normal distal and collecting tubules of the murine kidney. Lupus-like autoimmune disease and leukemia have been observed in SIPA-1 deficient mice, suggesting a pathological relevance of SIPA-1 to SLE and carcinoma in human being. The expression pattern of SIPA-1 is as yet undefined and the pathogenesis of these diseases in humans remains elusive. In this study, we used both immunohistochemistry and quantum dot (QD)-based immunofluorescence staining to investigate the expression of SIPA-1 in renal specimens from SLE and CC-RCC patients. MTT assay and Western blotting were employed to evaluate the effects of SIPA-1 overexpression on the proliferation and apoptosis of renal cell lines. Semi-quantitative reverse transcriptase-PCR (RT-PCR) was applied to examine the changes of hypoxia-inducible factor-1α (HIF-1α) mRNA level. Results showed that SIPA-1 was highly expressed in the proximal and collecting tubules of nephrons in SLE patients compared to normal ones, and similar results were obtained in the specimens of CC-RCC patients. Although SIPA-1 overexpression did not affect cellular proliferation and apoptosis of both human 786-O renal cell carcinoma cells and rat NRK-52E renal epithelial cell lines, RT-PCR results showed that HIF-1α mRNA level was down-regulated by SIPA-1 overexpression in 786-O cells. These findings suggest that SIPA-1 may play critical roles in the pathological changes in kidney, and might provide a new biomarker to aid in the diagnosis of SLE and CC-RCC.
- Published
- 2013
43. RETRACTED ARTICLE: Relationship of Serum Heart-Type Fatty Acid-Binding Protein Levels and Cerebral Infarction: a Meta-analysis
- Author
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Da-wei Li, Feng-ze Wang, Hui Yuan, Xiao-yi Yang, Cheng-Bi Zheng, Feng Zhang, Cun-Dong Fan, Jing-yi Sun, Zong-yong Zhang, Ming-feng Yang, Leilei Mao, Bao-liang Sun, and Hongli Gao
- Subjects
Cellular and Molecular Neuroscience ,medicine.medical_specialty ,Neurology ,business.industry ,Cerebral infarction ,Heart-type fatty acid binding protein ,Meta-analysis ,Neuroscience (miscellaneous) ,Medicine ,Pharmacology ,business ,medicine.disease - Published
- 2015
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