18 results on '"Wang, Di-Fen"'
Search Results
2. Epidemiology of methicillin-resistant Staphylococcus aureus infection and empirical antibiotic therapy for MRSA infection: multicenter investigation
- Author
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Deng, Li-jing, Wu, Xiao-dong, Kang, Yan, Xu, Yuan, Zhou, Jian-xin, Wang, Di-fen, and Chen, De-chang
- Published
- 2013
- Full Text
- View/download PDF
3. Risk factors prediction of 6-month mortality after noncardiac surgery of older patients in China: a multicentre retrospective cohort study.
- Author
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Wu XD, Wang Q, Song YX, Chen XY, Xue T, Ma LB, Luo YG, Li H, Lou JS, Liu YH, Wang DF, Wu QP, Peng YM, Mi WD, and Cao JB
- Subjects
- Humans, Aged, Retrospective Studies, Risk Assessment methods, Risk Factors, Clinical Decision-Making, Stroke
- Abstract
Background: Identifying the risk factors associated with perioperative mortality is crucial, particularly in older patients. Predicting 6-month mortality risk in older patients based on large datasets can assist patients and surgeons in perioperative clinical decision-making. This study aimed to develop a risk prediction model of mortality within 6 months after noncardiac surgery using the clinical data from 11 894 older patients in China., Materials and Methods: A multicentre, retrospective cohort study was conducted in 20 tertiary hospitals. The authors retrospectively included 11 894 patients (aged ≥65 years) who underwent noncardiac surgery between April 2020 and April 2022. The least absolute shrinkage and selection operator model based on linear regression was used to analyse and select risk factors, and various machine learning methods were used to build predictive models of 6-month mortality., Results: The authors predicted 12 preoperative risk factors associated with 6-month mortality in older patients after noncardiac surgery. Including laboratory-associated risk factors such as mononuclear cell ratio and total blood cholesterol level, etc. Also including medical history associated risk factors such as stroke, history of chronic diseases, etc. By using a random forest model, the authors constructed a predictive model with a satisfactory accuracy (area under the receiver operating characteristic curve=0.97)., Conclusion: The authors identified 12 preoperative risk factors associated with 6-month mortality in noncardiac surgery older patients. These preoperative risk factors may provide evidence for a comprehensive preoperative anaesthesia assessment as well as necessary information for clinical decision-making by anaesthesiologists., (Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc.)
- Published
- 2024
- Full Text
- View/download PDF
4. Role of dexmedetomidine in the treatment of delirium in critically ill patients: a systematic review and meta-analysis.
- Author
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Liu X, Xiong J, Tang Y, Gong CC, and Wang DF
- Subjects
- Adult, Bradycardia, Critical Illness, Humans, Delirium drug therapy, Dexmedetomidine therapeutic use
- Abstract
Introduction: Although dexmedetomidine has been found to prevent delirium in critically ill patients, it is uncertain whether it can treat acute delirium. This study aimed to evaluate the efficacy and safety of dexmedetomidine in treating delirium, by analyzing and reviewing data from previous studies., Evidence Acquisition: Clinical trial data on the use of dexmedetomidine in adult critically ill patients with delirium were retrieved from four databases (PubMed, Embase, Web of Science, and the Cochrane Library) and clinicaltrials.gov, from inception to May, 2020., Evidence Synthesis: Ten randomized controlled trials (RCTs) and five non-RCTs met the selection criteria and data were obtained from 1017 patients. In one study, dexmedetomidine reduced the duration of delirium to a greater extent than did the placebo. In six studies, it was associated with a lower point-prevalence of delirium after treatment (OR, 0.39; 95% CI, 0.20, 0.76; P=0.006) and a shorter time to resolution of delirium (hours; MD, -23.25; 95% CI, -45.28, -1.21; P=0.04) compared with those of other drugs. In four RCTs, it was superior to haloperidol in reducing the time to resolution of delirium (hours; MD, -30.17; P=0.01). However, in seven studies, it showed a higher risk of bradycardia (OR, 3.48; 95% CI, 1.47, 8.23; P=0.004) than that of comparators., Conclusions: Dexmedetomidine promotes the resolution of delirium but also increases the incidence of bradycardia during treatment. Furthermore, it may be superior to haloperidol in treating delirium, although more studies are needed to confirm this.
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- 2021
- Full Text
- View/download PDF
5. Attitudes, Knowledge, and Practices Regarding Blood Glucose Control: A Survey of Intensive Care Unit Professionals.
- Author
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Liu X, Wang DF, Liu Y, Tang Y, and Xiong J
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- Humans, Surveys and Questionnaires, Blood Glucose, Health Knowledge, Attitudes, Practice, Intensive Care Units
- Abstract
Competing Interests: There are no conflicts of interest.
- Published
- 2018
- Full Text
- View/download PDF
6. [Successful resuscitation of brain injury in a patient suffering from multiple organ injury due to electric injury: a case report].
- Author
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Huang DF and Wang DF
- Subjects
- Humans, Male, Middle Aged, Treatment Outcome, Brain Injuries therapy, Electric Injuries therapy, Multiple Trauma therapy, Resuscitation
- Published
- 2013
- Full Text
- View/download PDF
7. [Preventive effect of extracorporeal membrane oxygenation on complication during treatment of human infections with highly pathogenic avian influenza].
- Author
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Wang DF, Liu Y, Tang Y, Zeng XG, Liang XQ, Feng XY, and Song X
- Subjects
- Adult, Humans, Influenza A Virus, H1N1 Subtype, Influenza, Human virology, Ischemia prevention & control, Male, Extracorporeal Membrane Oxygenation adverse effects, Influenza, Human therapy, Ischemia etiology
- Published
- 2013
- Full Text
- View/download PDF
8. [The protective effect of propofol pretreatment on glutamate injury of neonatal rat brain slices].
- Author
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Zhou XF, Huang DD, Wang DF, and Fu JQ
- Subjects
- Animals, Brain metabolism, Brain pathology, L-Lactate Dehydrogenase metabolism, Neurons drug effects, Neurons metabolism, Rats, Rats, Sprague-Dawley, Tissue Culture Techniques, Brain drug effects, Glutamic Acid adverse effects, Propofol pharmacology
- Abstract
Objective: To study the protective effect of propofol precondition against glutamate (Glu) neurotoxicity to neonatal rat cerebrocortical slices., Methods: Brain slices of Sprague-Dawley (SD) rats were cultured in vitro and observed the morphologic changes. Brain slices were randomly divided into three groups: blank control group, Glu injury group (1 mmol/L Glu for 0.5 hour), propofol precondition group (20 mg/L propofol for 24 hours), each n=12. Changes in pathological and ultra-structure of cells were observed using microscope. Lactate dehydrogenase (LDH) leakage rate was measured. Meanwhile, the expression of glial fibrillary acidic protein (GFAP) was detected by immunohistochemical technology, then the positive cell were counted., Results: Cultured brain slices of cell were intact and survived well. Hematoxylin-eosin (HE) staining, electron microscopy and LDH test results showed that cerebral film neuron severely damage, gliosis, edema, LDH leakage rate in Glu injury group were significantly more severe compared with blank control group [(68.5±2.0)% vs. (16.0±2.5)%, P<0.01]. Reduce the brain slice of the propofol pretreatment group of neuronal cell jury, cell shape recovery significantly reduced LDH leakage rate compared with the Glu injury group [(38.5±2.4)% vs. (68.5±2.0)%, P<0.05]. Immunohistochemical detection of GFAP expression of Glu injury group glial cell body swelling, producing increase in the number of GFAP positive reaction strong, the number of positive cells compared with blank control group was significantly increased (50±5 cells/HP vs. 10±3 cells/HP, P<0.01). The recovery of propofol pretreatment group glial cell morphology, cell processes slender GFAP positive reaction decreased the number of positive cells compared with the Glu injury group was significantly decreased (30±4 cells/HP vs. 50±5 cells/HP, P<0.05)., Conclusion: Propofol pretreatment has protective effect against Glu injured rat cerebrocortical slices.
- Published
- 2012
9. [Neonatal rat cerebral cortical neurons culture method].
- Author
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Yao N, Wang DF, Song X, and Liu XL
- Subjects
- Animals, Cell Culture Techniques, Cells, Cultured, Rats, Rats, Sprague-Dawley, Cerebral Cortex cytology, Neurons cytology
- Published
- 2012
10. [Prospective observational study exploring the relationship between the levels and variability of blood glucose and the prognosis of critical patients].
- Author
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Liu X, Wang DF, and Xiong J
- Subjects
- APACHE, Adult, Aged, Aged, 80 and over, Female, Humans, Intensive Care Units, Male, Middle Aged, Prognosis, Prospective Studies, Young Adult, Blood Glucose metabolism, Hospital Mortality
- Abstract
Objective: To explore the relationship between the levels and variability of blood glucose and the prognosis of critical patients., Methods: A prospective study was conducted. Blood glucose monitoring and prognosis observation were performed for the adult nondiabetic patients admitted in intensive care unit (ICU) from June 2011 to January 2012. Blood glucose monitoring terminal was 72 hours after admitting in ICU, prognosis was observed for 28 days after the end of turning into ICU. Acute physiology and chronic health evaluation II(APACHE II) scores when transferred into ICU and blood glucose variability [standard deviation (SD) of blood glucose, mean absolute blood glucose fluctuation amplitude (MAGE) and glycemic instability index (GLI)] were calculated. Patients were divided into death group and survival group according to the outcome, and the APACHE II score, mean blood glucose and blood glucose variability were compared between the two groups. Patients were divided into different groups based on the blood glucose, and the APACHE II score, blood glucose variability and 28-day mortality were compared among groups., Results: Total 85 cases were enrolled. Compared with survivor group (n=58), in death group (n=27), APACHE II score (28.9±6.6 vs. 23.8±5.9), mean blood glucose (11.9±2.9 mmol/L vs. 9.4±1.8 mmol/L), SD of blood glucose (3.7±1.6 mmol/L vs. 2.4±1.0 mmol/L), MAGE (0.86±0.46 mmol/L vs. 0.54±0.25 mmol/L) and GLI (255.9±232.7 vs. 111.7±110.9) were increased (all P<0.05). SD of blood glucose (4.3±1.4 mmol/L), MAGE (1.1±0.4 mmol/L), GLI (345.3±210.3) and 28-day mortality (63.6%) in blood glucose >11.1 mmol/L group (n=22) were higher than those in ≤11.1 mmol/L group (n=63, 2.3±0.9 mmol/L, 0.5±0.2 mmol/L, 91.9±91.2, 20.6%, respectively, all P<0.05) and 7.8-11.1 mmol/L group (n=52, 2.3±0.9 mmol/L, 0.5±0.2 mmol/L, 85.2±66.4, 25.0%, respectively, all P<0.05). There were no significant differences between 7.8-11.1 mmol/L group and <7.8 mmol/L group (n=11) in SD of blood glucose (2.0±0.9 mmol/L), MAGE (0.5±0.3 mmol/L), GLI (123.8±166.7) and 28-day mortality (0, all P>0.05)., Conclusion: Blood glucose variability is associated with critical patient's 28-day mortality, and may predict mortality as good as APACHE II score.
- Published
- 2012
11. [Neuroprotective effects of combined pretreatment with edaravone and propofol on neonatal rat cerebral cortical neurons with ischemia/reperfusion injury in vitro].
- Author
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Yao N, Wang DF, Song X, and Liu XL
- Subjects
- Animals, Antipyrine pharmacology, Antipyrine therapeutic use, Apoptosis, Brain Ischemia prevention & control, Cell Survival, Cells, Cultured, Cerebral Cortex blood supply, Cerebral Cortex drug effects, Edaravone, Neuroprotective Agents therapeutic use, Propofol therapeutic use, Rats, Rats, Sprague-Dawley, Reperfusion Injury prevention & control, Antipyrine analogs & derivatives, Cerebral Cortex cytology, Neurons drug effects, Neuroprotective Agents pharmacology, Propofol pharmacology
- Abstract
Objective: To investigate the protective effect of combined pretreatment of edaravone and propofol on cerebral cortex with ischemia/reperfusion (I/R) injury and its therapeutic window., Methods: Sprague Dawley (SD) rat brain cortex cells harvested within 24 hours of birth were cultured in vitro for 7 days. The cells were then divided into blank control group, glutamate injury group, 24-hour drug precondition control group, and 24-, 2-, 0-hour drug precondition groups according to random number table. The nerve cells in each pretreatment group were cultured in medium containing 100 μmol/L of edaravone and 3 mg/L of propofol 24, 2, or 0 hour before glutamate damage (200 μmol/L for 0.5 hour). Nerve cell survival or damage was determined by methyl thiazolyl tetrazolium (MTT), lactate dehydrogenase (LDH) leakage rate, and nerve cell Na+-K+-ATPase activity. The oxidation and anti-oxidation ability of nerve cells was observed by determining superoxide dismutase (SOD) activity (xanthine oxidase), malondialdehyde (MDA) content (thiobarbituric acid). Nerve apoptosis was detected by flow cytometry., Results: Compared with blank control group, in the glutamate injury group, nerve cell survival rate [(62.2±23.4)% vs. (90.5±14.8)%], the activity of SOD (U/ml: 6.864±2.872 vs. 29.569±3.684), Na+-K+-ATPase activity [U×mg(-1)×h(-1): 0.318±0.146 vs. 0.636±0.168] were significantly decreased, and rate of neuronal apoptosis [(9.4±0.7)% vs. (6.1±0.2)%], the content of MDA (nmol/ml: 0.515±0.101 vs. 0.294±0.105), LDH leakage rate [(41.2±1.6)% vs. (36.8±4.6)%] were significantly increased (P<0.05 or P<0.01). Compared with glutamate injury group, the cell survival rate and the activity of SOD and Na+-K+-ATPase were significantly increased in the drug pretreatment groups, and apoptosis rate, MDA content, and LDH leakage rate were significantly decreased with time-department, and effect in the 24-hour pretreatment group was most significant [survival rate of cell: (89.2±30.3)% vs. (62.2±23.4)%, SOD activity (U/ml): 17.780±4.514 vs. 6.864±2.872, Na+-K+-ATPase activity [U×mg(-1)×h(-1)]: 0.541±0.052 vs. 0.318±0.146, the rate of cell apoptosis: (6.7±0.4)% vs. (9.4±0.7)%, the content of MDA (nmol/ml): 0.319±0.101 vs. 0.515±0.101, LDH leakage rate: (37.2±1.4)% vs. (41.2±1.6)%, all P<0.01]., Conclusion: The synergistic protective effect of pretreatment with edaravone combined with propofol on neonatal rat brain cortex cells with I/R injury in vitro was evident; and 24-hour pretreatment is the best time window of protection for the cerebral neurons.
- Published
- 2012
12. [A comparative study on the protection effect of nerve growth factor and edaravone pretreatment against cerebral ischemia/reperfusion injury].
- Author
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Fu JQ, Wang DF, and Liu H
- Subjects
- Animals, Animals, Newborn, Antipyrine therapeutic use, Apoptosis drug effects, Brain Ischemia pathology, Cells, Cultured, Disease Models, Animal, Edaravone, Free Radical Scavengers therapeutic use, Neurons drug effects, Neurons pathology, Rats, Rats, Sprague-Dawley, Reperfusion Injury pathology, Antipyrine analogs & derivatives, Brain Ischemia prevention & control, Nerve Growth Factor therapeutic use, Reperfusion Injury prevention & control
- Abstract
Objective: To compare the protective effect of nerve growth factor (NGF) and edaravone (a free radical scavenger) pretreatment against cerebral ischemia/reperfusion (I/R) injury to nerve cells., Methods: Cortical neurons of Sprague-Dawley (SD) mouse aged shorter than 24 hours were cultured for 7 days, then they were randomly divided into control group, I/R group, NGF of 10, 50, 100 microg/L pretreatment groups and 100 mumol/L edaravone pretreatment group. In pretreatment groups the cells were pretreated with drugs correspondingly. After culturing for 24 hours, glutamate of 200 mumol/L was given into the culture of all groups, except control group, for half an hour. Then culture medium in all groups were renewed with ordinary culture medium, and cultures were continued for 24 hours. The survival rate (by methyl thiazolyl tetrazolium assay), the content of lactate dehydrogenase (LDH, by spectrometry) and the rate of apoptosis (by flow cytometric) were determined. The cellular shape and ultrastructure were observed by hematoxylin-eosin (HE) staining and electronic microscopy correspondingly., Results: The survival rate of nerve cells in NGF groups and edaravone group was significantly higher than that in I/R group [(0.21 + or - 0.04)%, (0.23 + or - 0.04)%, (0.21 + or - 0.04)%, (0.24 + or - 0.04)% vs. (0.19 + or - 0.04)%]. The content of LDH in culture medium and the rate of apoptosis in NGF groups and edaravone group were lower than those in I/R group (P<0.05 or P<0.01). The release rate of LDH in each group was (0.50 + or - 0.06)%, (0.46 + or - 0.07)%, (0.50 + or - 0.02)%, (0.43 + or - 0.06)% vs. (0.56 + or - 0.03)%, respectively. The rate of apoptosis in each group was (10.77 + or - 1.07)%, (10.38 + or - 0.70)%, (13.34 + or - 0.57)%, (9.99 + or - 0.77)% vs. (14.52 + or - 0.77)%, respectively. The cellular shape and ultrastructure of nerve cells in NGF groups and edaravone group were affected much less than that of I/R group. NGF of 50 microg/L pretreatment group gave the best effect among three groups. There was no significant difference between NGF 50 microg/L pretreatment group and edaravone pretreatment group., Conclusion: NGF and edaravone pretreatment 24 hours before cerebral I/R give protective effects against cerebral I/R injury. The protective effects are best in NGF of 50 microg/L pretreatment group and edaravone pretreatment group, and there is no significant difference between them.
- Published
- 2010
13. [A study of the protective effects of lidocaine and nerve growth factor pretreatment on cerebral ischemia/reperfusion injury in gerbils].
- Author
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Xie JD and Wang DF
- Subjects
- Animals, Apoptosis drug effects, Brain Ischemia pathology, Disease Models, Animal, Gerbillinae, Ischemic Preconditioning, Neurons pathology, Reperfusion Injury pathology, Brain Ischemia prevention & control, Lidocaine therapeutic use, Nerve Growth Factor therapeutic use, Reperfusion Injury prevention & control
- Abstract
Objective: To study the protective effects of lidocaine and nerve growth factor (NGF) pretreatment on cerebral ischemia/reperfusion (I/R) injury., Methods: Fifty-four Mongolian gerbils were randomly divided into nine groups: normal group (Group A), lidocaine control group (Group L), NGF control group (Group N), lidocaine pretreatment groups at the point of 12, 24, 48 hours (named respectively Group L12, L24, L48), NGF pretreatment groups with NGF given 12, 24, 48 hours before injury (named respectively Group N12, N24, N48), with 6 animals in each group. Except Group A, the carotid artery on both sides were occluded for 20 minutes, then they were released to allow reperfusion. Alteration of apoptosis was observed with terminal-deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) and the expression of Bcl-2 and Bax was assessed by immunohistochemistry method., Results: No apoptosis, Bcl-2 and Bax were found in Group A. In lidocaine or NGF pretreatment group, the expression of Bcl-2 (Group L12: 36.60 + or - 3.31, Group L24: 34.73 + or - 1.82, Group L48: 65.17 + or - 1.53; Group N12: 35.70 + or - 1.18 , Group N24: 37.30 + or - 3.86, Group N48: 62.77 + or - 2.91) was obviously increased comparing with control group (Group L: 24.53 + or - 1.48, Group N: 25.43 + or - 1.85), but the number of the apoptosis (Group L12: 32.87 + or - 0.99, Group L24: 31.90 + or - 4.14, Group L48: 24.50 + or - 0.70; Group N12: 32.80 + or - 1.27, Group N24: 32.83 + or - 1.30, Group N48: 23.30 + or - 0.86) and Bax expression (Group L12: 33.47 + or - 1.21, Group L24: 33.70 + or - 1.20, Group L48: 24.67 + or - 2.09; Group N12: 32.17 + or - 2.21, Group N24: 31.97 + or - 1.79, Group N48: 23.27 + or - 1.20) were significantly decreased comparing with the control group (the number of the apoptosis: Group L 67.43 + or - 3.92, Group N 67.80 + or - 3.82; Bax: Group L 59.73 + or - 1.32, Group N 59.37 + or - 1.54, P<0.05 or P<0.01). In lidocaine and NGF pretreatment groups, the number of cell apoptosis and expression Bax were significantly lower at 48 hours than those at 12 hours or 24 hours, but the cell expression Bcl-2 was obviously higher (all P<0.05). However, there was no difference between lidocaine and NEG pretreatment groups at each time point in regard of the number of cell apoptosis, expression of Bcl-2 and Bax., Conclusion: Lidocaine and NGF pretreatment before cerebral I/R can alleviate I/R injury to the cerebral tissue. The protective effect was most obvious when the treatment was given 48 hours before ischemia. The mechanism may be related with an increase in expression of Bcl-2 as well as a decrease in Bax level.
- Published
- 2010
14. [Experience of diagnosis and treatment of ventilator-associated lung injury].
- Author
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Liu Y, Fu JQ, Wang Y, and Wang DF
- Subjects
- Acute Lung Injury etiology, Adult, Female, Humans, Male, Middle Aged, Acute Lung Injury diagnosis, Acute Lung Injury therapy, Respiration, Artificial adverse effects
- Published
- 2009
15. [Protective effect of lidocaine on glutamic acid induced neuronal injury in rat].
- Author
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Han AL, Wang DF, Mei Z, Liu XM, Liu XL, and Wu CL
- Subjects
- Animals, Cells, Cultured, Drug Antagonism, Neurons drug effects, Rats, Rats, Sprague-Dawley, Glutamic Acid toxicity, Lidocaine pharmacology, Neurons pathology
- Published
- 2008
16. [A comparison of protective effect of propofol and edaravone pretreatment against cerebral ischemia-reperfusion injury].
- Author
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Liu H, Wang DF, and Fu JQ
- Subjects
- Animals, Antipyrine pharmacology, Apoptosis, Brain Ischemia prevention & control, Cell Survival, Cells, Cultured, Cerebral Cortex cytology, Edaravone, Neurons drug effects, Neurons metabolism, Rats, Reperfusion Injury prevention & control, Antipyrine analogs & derivatives, Neurons pathology, Propofol pharmacology
- Published
- 2008
17. [Protective effect of verapamil pretreatment against cerebral ischemia-reperfusion injury in gerbils].
- Author
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Ding N, Wang F, Xiao H, and Wang DF
- Subjects
- Animals, Brain drug effects, Brain metabolism, Brain pathology, Brain Ischemia metabolism, Brain Ischemia pathology, Endothelins metabolism, Gerbillinae, Glutathione metabolism, Malondialdehyde metabolism, Receptors, Calcitonin Gene-Related Peptide metabolism, Reperfusion Injury metabolism, Reperfusion Injury pathology, Superoxide Dismutase metabolism, Brain Ischemia complications, Brain Ischemia prevention & control, Reperfusion Injury complications, Reperfusion Injury prevention & control, Verapamil pharmacology
- Abstract
Objective: To observe the protective effect of verapamil pretreatment against cerebral ischemia-reperfusion injury in gerbils., Methods: Thirty-three Mongolian gerbils were randomized into the control group (group A, n=6, with sham operation), ischemia group (group B), and 3 verapamil groups (groups C, D, and E, n=7) with intraperitpneal verapamil injection (2 mg/kg) 48, 24 and 12 h before ischemia, respectively. In group A, the bilateral common carotid arteries were only exposed without clamping, and in the other 4 groups, the arteries were clamped for 20 min followed by reperfusion for 50 min. The gerbils were then decapitated and the forebrain cerebral cortex was removed to determine superoxide dismutase (SOD) and glutathione (GSH) activities and measure the contents of malondial dehyde (MDA), endothelin (ET) and calcitonin gene-related peptide (CGRP). The left forebrain cerebral cortex was sampled in each group to observe the ultrastructural changes under electron microscope., Results: In groups C and D, SOD activities were significantly higher than those in group B (P<0.05), and in group E, the SOD activity elevation was not statistically significant (P>0.05). In groups C, D and E, GSH activity was significantly higher than that in group B (P<0.05). MDA content was significantly lower in groups C and D than in group B (P<0.05), but comparable between groups E and B (P>0.05). ET content was also significantly lower in the pretreatment groups (P<0.05), but CGRP content higher (not statistically so, however) than those in group B. The more serious ultrastructural damage of the cerebral tissue was observed in group B, but only mild damage was found in the verapamil groups., Conclusions: Verapamil given 12-48 h before cerebral ischemia may protect the gerbils from cerebral ischemia-reperfusion injury by enhancing SOD, GSH activities and decreasing ET content.
- Published
- 2007
18. [Effects of nerve growth factor pretreatment on apoptosis of neurons and expression of Bcl-2, Bax protein in brain tissue following cerebral ischemia/reperfusion injury in gerbils].
- Author
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Tan YX, Wang DF, Li XM, and Liu XM
- Subjects
- Animals, Brain Ischemia metabolism, Disease Models, Animal, Female, Gerbillinae, Hippocampus drug effects, Hippocampus metabolism, Hippocampus pathology, Male, Neurons drug effects, Neurons metabolism, Proto-Oncogene Proteins c-bcl-2 metabolism, Random Allocation, Reperfusion Injury metabolism, bcl-2-Associated X Protein metabolism, Apoptosis drug effects, Brain Ischemia pathology, Nerve Growth Factor pharmacology, Neurons pathology, Reperfusion Injury pathology
- Abstract
Objective: To study the effect of nerve growth factor (NGF) pretreatment on apoptosis of neurons and the expression of Bcl-2 and Bax protein in cerebral cortex and hippocampus CA1 zone following global cerebral ischemia/reperfusion (I/R) injury in gerbils and to explore the mechanism of protection and the best time window of NGF pretreatment., Methods: Global cerebral I/R injury model was induced by occlusion of bilateral carotid arteries. NGF was injected into the lateral ventricle. Thirty gerbils were randomly divided into five groups, with six animals in each: sham operation group (A group), I/R injury group (B group), NGF pretreatment 12, 24 and 48 hours groups (C, D and E group). Gerbils in all groups were sacrificed after being subjected to 20 minutes of cerebral ischemia followed by 72 hours reperfusion, except A group. Neural apoptosis was identified by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL), and immunohistochemistry was used to detect the expression of Bcl-2 and Bax protein in cerebral cortex and hippocampus CA1 zone., Results: Compared with B group, the number of apoptotic neurons and the expression of Bax positive cells in NGF pretreatment groups were decreased significantly (all P<0.05), while the expression of Bcl-2 positive cells was increased significantly (all P<0.05). The apoptotic rate in cerebral cortex and hippocampus CA1 zone and expression rate of Bax protein positive cells were the lowest, but the expression rate of Bcl-2 protein positive cells was the highest at 48 hours., Conclusion: NGF pretreatment can significantly decrease the neuronal apoptosis of the cerebral I/R injury in gerbils, and the best time window of NGF pretreatment is 48 hours. The mechanism of protection may be related to induction of Bcl-2 protein expression and inhibition of Bax protein expression by NGF pretreatment, thereby preventing neuronal apoptosis.
- Published
- 2007
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