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Objective:To investigate the effect of oxycodone hydrochloride injection pretreatment on focal cerebral ischemia-reperfusion injury in rats.Methods:Seventy-two male SD rats weighing 200-250 g were randomly divided into 3 groups( n=24 each group): sham operation group (sham group), focal cerebral I/R group (I/R group), and oxycodone hydrochloride injection group (Oxy group). Focal cerebral I/R was induced by middle cerebral artery occlusion for 2 h followed by reperfusion. In the Oxy group, oxycodone hydrochloride 0.5 mg/kg was injected iv at 5 min before ischemia. While the same volume of saline (1 mL) was injected in the sham group and I/R group. The neurological deficit score (NDS) was assessed at 24 h of reperfusion, the rats were then sacrificed, and their brains were immediately removed for determination of brain water content and the infarct volume, and the histopathological changes were observed after HE staining. The levels of cytokines (TNF-α, IL-1β and IL-10) in the ischemia cortex were quantified by ELISA. MPO activity in the ischemia cortex was assessed. Western blot was used to detect the expression of NF-κB in the ischemia cortex. The data were analyzed using SPSS 20.0 software, multiple-group comparisons were performed using one-way ANOVA, and LSD- t test was used for pairwise comparison between groups. A P<0.05 was considered statistically significant different. Results:Compared with the sham group, NDS, brain water content, relative infarction volume and rate of nerve cell necrosis were significantly increased in the I/R and Oxy groups (all P<0.05). Levels of TNF-α, IL-1β, IL-10, NF-κB and the activities of MPO were increased in the ischemia cortex (all P<0.05). Compared the Oxy group with the I/R group, NDS, brain water content, relative infarction volume and rate of nerve cell necrosis were significantly decreased [(1.7±0.9) vs (2.6±1.1);(79.2±2.4)% vs (84.7±4.2)%; (23.0±5.4)% vs (34.8±6.0)%; (25.2±12.4)% vs (54.8±14.8)%, all P<0.05]. The levels of TNF-α, IL-1β, relative expression of NF-κB, and the activities of MPO were significantly decreased in the ischemia cortex [(4.4±1.2) pg/mg vs (6.5±1.2) pg/mg; (5.4±0.7) pg/mg vs (7.8±0.8) pg/mg; (0.83±0.11) vs (1.23±0.33); (0.27±0.09) U/g vs (0.36±0.14) U/g, all P<0.05] , while the concentration of IL-10 was significantly increased [(20.9±4.5) pg/mg vs (9.2±1.6) pg/mg, t=6.036, P=0.000 1]. Conclusions:Oxycodone hydrochloride can attenuate focal cerebral I/R injury through inhibiting NF-κB activity.
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OBJECTIVE: To analyze the current situation and correlation between job burnout and mental health of college counselors in Shanghai City. METHODS: With stratified cluster random sampling method, 235 counselors were selected as study subjects. Their job burnout and mental health was investigated by using Burnout Inventory Educator's Survey and Kessler Psychological Distress Scale. RESULTS: The median score of the 3 dimensions of emotional exhaustion, deindividualization and low sense of achievement of counselors was 3.4, 3.2 and 1.6, respectively. In each dimension, the ratio of moderate level job burnout was 93.2%, 94.9% and 26.8%, respectively; the ratio of high level job burnout was 6.8%, 5.1% and 73.2%, respectively. The median score of mental health was 31.0, and the grade of general, poor and very poor mental health standard was 2.6%, 35.3% and 62.1%, respectively. The scores of emotional exhaustion and deindividualization were positively correlated with the scores of mental health status(Spearman correlation coefficients were 0.54 and 0.44, all P<0.01). The score of low achievement was negatively correlated with the score of mental health status(Spearman correlation coefficient=-0.39, P<0.01). The multiple linear regression analysis showed that the scores of emotional exhaustion and deindividualization had positive predictive value on mental health after excluding gender, spouse, age, length of service, educational level, position title, household registration, authorized strength, and university level(all P<0.01). Low achievement score had a negative predictive effect on mental health(P<0.01). CONCLUSION: The job burnout in college counselors in Shanghai City is at a moderately high level and their mental health is poor. The job burnout affects their mental health. Alleviating job burnout is beneficial to improve counselors′ mental health.
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OBJECTIVE: To analyze the relationship between health promoting lifestyle and job burnout of college counselors in Shanghai. METHODS: Using stratified cluster sampling method, 294 counselors from 4 colleges were selected and investigated by Maslach Burnout Inventory Educator's Survey and Health Promoting Lifestyle Profile II. RESULTS: The median scores of emotional exhaustion, deindividualization and low sense of achievement of counselors in Shanghai were 3.3, 3.2 and 1.6 respectively. In each dimension, the ratio of moderate burnout were 93.5%, 95.2% and 26.5% respectively. The ratio of high level burnout were 6.5%, 4.8% and 73.5%. The median total score of health promoting lifestyle was 127.1, and the ratio of poor, average and good lifestyle standard was 8.5%, 50.3% and 41.2%.The total score of health promoting lifestyle was negatively correlated with the score of emotional exhaustion and deindividualization(P<0.01) and positively correlated with the score of low sense of achievement(P<0.01). The score of physical exercise, interpersonal relationship, stress management and self realization in health promoting lifestyle had positive predictive effect on the score of emotional exhaustion and deindividualization(P<0.05). The score of physical exercise and self realization had negative predictive effect on the score of low sense of achievement(P<0.01). CONCLUSION: The prevalence of job burnout in college counselors is above the intermediate level. There is a correlation between health promoting lifestyle and job burnout and cultivating a health promoting lifestyle is helpful to alleviate job burnout.
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Objective@#This study aimed to evaluate the clinical performance of p16/Ki-67 dual staining for triage high risk HPV (HR-HPV) infected women.@*Method@#Target objects were women who infected HR-HPV and received colposcopy examination between April and December of 2016 at the Second Affiliated Hospital of Zhengzhou University. Gynecologists collected the cervical exfoliated cells from eligible women for p16/Ki-67 dual staining, LBC testing and HPV DNA testing. Histology diagnosis were used as gold standard. Sensitivities, specificities, positive predictive values (PPVs), negative predictive values (NPVs) of p16/Ki-67 dual staining, LBC testing and HPV16/18 testing for triage of HR-HPV positive population were calculated and compared.@*Results@#A total of 295 HR-HPV infected women were selected, and the mean age was (44.29±11.48) years old. Positive rates of p16/Ki-67 dual staining, HPV16/18 testing and LBC testing were 70.17% (207), 56.95% (168) and 85.76% (253), respectively. When CIN2+as the endpoint, among the three triage methods, sensitivity of p16/Ki-67 dual staining was 90.00% (95%CI: 85.06%-93.43%), higher than the value of HPV 16/18 testing, but lower than the value of LBC testing. Specificity, PPV and NPV of p16/Ki-67 dual staining were the highest [71.58% (95%CI: 61.81%-79.67%), 86.96% (95%CI:81.69%-90.88%) and 77.27% (95%CI: 67.49%-84.78%)]. When detection for CIN3+, sensitivity of p16/Ki-67 dual staining was 92.90% (95%CI: 87.74%-95.99%), lower than the value of LBC testing, but higher than the value of HPV16/18 testing. Specificity of p16/Ki-67 dual staining was 55.00% (95%CI: 46.74%-63.00%), lower than the value of HPV16/18 testing, but higher than the value of LBC testing. PPV of p16/Ki-67 dual staining was 69.57% (95%CI: 62.99%-75.43%), lower than the value of HPV 16/18 testing, but higher than the value of LBC testing. NPV of p16/Ki-67 dual staining was 87.50% (95%CI: 78.99%-92.87%), higher than value of HPV 16/18 testing, but lower than the value of LBC testing.@*Conclusion@#p16/Ki-67 dual staining has better clinical effects than HPV 16/18 testing and LBC testing for triage women with HR-HPV infection.
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OBJECTIVE@#To investigate the effects of different doses of propofol on myelin basic protein (MBP) synthesis and myelination of oligodendrocytes in neonatal SD rats.@*METHODS@#A total of 57 neonatal SD rats (7 days old) were randomly divided into control group (=13), vehicle (fat emulsion) group (=5), and 25, 50 and 100 mg/kg propofol groups (=13 in each group). Eight hours after a single intraperitoneal injection of propofol or the vehicle, the rats were examined for expressions of mRNA, caspase-3 mRNA, cleaved caspase-3 and MBP in the brain tissues using qPCR and Western blotting. Immunofluorescence assay was used to detect the apoptosis of the oligodendrocytes at 8 h after the injection and the myelination of the corpus callosum and internal capsule at 24 h.@*RESULTS@#Compared with the control group, the neonatal rats with propofol injections showed significantly down-regulated expressions of mRNA and MBP protein in the brain tissue ( < 0.05). Propofol dose-dependently increased the transcription level of caspase-3 and the protein levels of cleaved caspase-3 at 8 h after the injection ( < 0.05). Propofol injection significantly increased the apoptosis of the oligodendrocytes, and the effect was significantly stronger in 50 and 100 mg/kg groups than in 25 mg/kg group ( < 0.05). At 24 h after propofol injection, myelin formation was significantly decreased in the corpus callosum of the neonatal rats in 100 mg/kg propofol group and in the internal capsule in 50 and 100 mg/kg groups ( < 0.05).@*CONCLUSIONS@#In neonatal SD rats, propofol can dose-dependently promote oligodendrocyte apoptosis, decrease MBP expressions in the brain, and suppress myelin formation in the corpus callosum and the internal capsule.
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Animals , Rats , Myelin Basic Protein , Oligodendroglia , Propofol , RNA, Messenger , Rats, Sprague-DawleyABSTRACT
Objective@#To evaluate the effect of irisin preconditioning on global cerebral ischemia-reperfusion (I/R) injury in rats.@*Methods@#Thirty-six healthy male Sprague-Dawley rats, aged 8-10 weeks, weighing 250-300 g, were divided into 3 groups (n=12 each) using a random number table method: sham operation group (group S), global cerebral I/R group (group I/R) and irisin preconditioning group (group I). Global cerebral I/R was induced by occlusion of bilateral common carotid arteries combined with hypotension (MAP maintained at 35-45 mmHg) in anesthetized rats.At 30 min before ischemia, irisin 10 μg/kg (diluted to 10 μg/ml in normal saline) was intravenously injected in group I, and the equal volume of normal saline was intravenously injected in S and I/R groups.Morris water maze test was performed at day 3 of reperfusion to assess the cognitive function.Rats were sacrificed after the end of morris water maze test, and brains were removed for determination of histopathologic changes in hippocampal CA1 region (using HE staining), neuronal apoptosis in hippocampal CA1 region (Tunel staining), glial fibrillary acidic protein (GFAP) expression (by Western blot), myeloperoxidase (MPO) activity in the hippocampal tissues (by colorimetric assay), and contents of tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-1β) in hippocampal tissues (by enzyme-linked immunosorbent assay). The cell necrosis rate and apoptotic rate were calculated.@*Results@#Compared with group S, the escape latency was significantly prolonged on 1-5 days in group I/R and on 1-3 days in group I, the time of staying at 1st quadrant was significantly shortened, the cell necrosis rate and apoptotic rate were increased, the expression of GFAP was up-regulated, and the activity of MPO and contents of TNF-α and IL-1β were increased in I/R and I groups (P<0.05 or 0.01). Compared with group I/R, the escape latency was significantly shortened on 1-5 days, the time of staying at 1st quadrant was prolonged, the cell necrosis rate and apoptotic rate were decreased, the expression of GFAP was down-regulated, and the MPO activity and contents of TNF-α and IL-1β were decreased in group I (P<0.05 or 0.01).@*Conclusion@#Irisin preconditioning can reduce the global cerebral I/R injury in rats, and the mechanism may be related to inhibiting activation of astrocytes in hippocampus and reducing inflammatory responses.
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Objective To evaluate the effect of irisin preconditioning on global cerebral ischemiareperfusion (I/R) injury in rats.Methods Thirty-six healthy male Sprague-Dawley rats,aged 8-10 weeks,weighing 250-300 g,were divided into 3 groups (n=12 each) using a random number table method:sham operation group (group S),global cerebral I/R group (group I/R) and irisin preconditioning group (group I).Global cerebral I/R was induced by occlusion of bilateral common carotid arteries combined with hypotension (MAP maintained at 35-45 mmHg) in anesthetized rats.At 30 min before ischemia,irisin 10 μg/kg (diluted to 10 μg/ml in normal saline) was intravenously injected in group I,and the equal volume of normal saline was intravenously injected in S and I/R groups.Morris water maze test was performed at day 3 of reperfusion to assess the cognitive function.Rats were sacrificed after the end of morris water maze test,and brains were removed for determination of histopathologic changes in hippocampal CA1 region (using HE staining),neuronal apoptosis in hippocampal CA1 region (Tunel staining),glial fibrillary acidic protein (GFAP) expression (by Western blot),myeloperoxidase (MPO) activity in the hippocampal tissues (by colorimetric assay),and contents of tumor necrosis factor-alpha (TNF-cα) and interleukin-1 beta (IL-1β) in hippocampal tissues (by enzyme-linked immunosorbent assay).The cell necrosis rate and apoptotic rate were calculated.Results Compared with group S,the escape latency was significantly prolonged on 1-5 days in group I/R and on 1-3 days in group I,the time of staying at 1st quadrant was significantly shortened,the cell necrosis rate and apoptotic rate were increased,the expression of GFAP was up-regulated,and the activity of MPO and contents of TNF-α and IL-1β were increased in I/R and I groups (P＜0.05 or 0.01).Compared with group I/R,the escape latency was significantly shortened on 1-5 days,the time of staying at 1st quadrant was prolonged,the cell necrosis rate and apoptotic rate were decreased,the expression of GFAP was down-regulated,and the MPO activity and contents of TNF-α and IL-1β were decreased in group I (P＜0.05 or 0.01).Conclusion Irisin preconditioning can reduce the global cerebral I/R injury in rats,and the mechanism may be related to inhibiting activation of astrocytes in hippocampus and reducing inflammatory responses.
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The temporoparietal fascia (TPF) is a robust and distinct layer between the deep temporal fascia and the subcutaneous fat in the temporal region. The TPF is richly vascularized by superficial temporal vessels. Besides, its thin and pliable characteristics with secluded incision and minimal donor site morbidity provide a good option for the plastic and reconstructive surgeons. Recently, the TPF flap was employed to treat some rare diseases such as the laryngotracheal stenosis and pharyngocutaneous fistula. This article extensively reviewed relevant researches on the application of the fascial flaps in recent years.
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<p><b>OBJECTIVE</b>To investigate the mechanism underlying propofol- induced down-regulation of myelin basic protein (MBP) in zebrafish embryos.</p><p><b>METHODS</b>Zebrafish embryos (6-48 h post-fertilization [hpf]) were randomized into 4 equal groups for exposure to dimethyl sulfoxide (DMSO), 20 μg/mL propofol, 30 μg/mL propofol, or no particular treatment (control group). The larvae were collected at 48 or 72 hpf for detecting the mRNA levels of MBP, Olig1, Olig2, and Sox10 using qRT-PCR (=80). The protein expression of MBP was quantitatively detected using Western blotting (=80), and the apoptosis of the oligodendrocytes was investigated using TUNEL staining (=6).</p><p><b>RESULTS</b>Exposure to 20 and 30 μg/mL propofol caused significant reductions in the mRNA expressions of Olig1, Olig2, and Sox10 at 48 and 72 hpf ( < 0.05) and also in MBP mRNA and protein levels at 72 hpf ( < 0.05). Exposure to 30 μg/mL propofol induced more obvious reduction in MBP protein expression than 20 μg/mL propofol at 72 hpf ( < 0.05), and the exposures resulted in a significant increase of oligodendrocyte apoptosis at 72 hpf ( < 0.05).</p><p><b>CONCLUSIONS</b>Propofol exposure reduces MBP expression at both the mRNA and protein levels in zebrafish embryos by down-regulating the expressions of Olig1, Olig2 and Sox10 mRNA levels and increasing apoptosis of the oligodendrocytes.</p>
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Objective To evaluate the effect of quercetin pretreatment on the permeability of blood-brain barrier in a rat model of global cerebral ischemia-reperfusion ( I∕R). Methods Sixty-three clean-grade healthy male Sprague-Dawley rats, weighing 300-350 g, aged 4-5 months, were divided into 3 groups (n＝21 each) using a random number table method: sham operation group ( group S), group I∕R and quercetin pretreatment group ( group Q). Global cerebral I∕R was induced by occlusion of bilateral common carotid arteries combined with hypotension ( mean arterial pressure was maintained at 35-45 mmHg) in chloral hydrate-anesthetized rats. Quercetin 25 μmol∕kg was injected intraperitoneally twice a day for 3 consecutive days starting from 3 days before establishment of the model in group Q, while the e-qual volume of normal saline was given instead at the corresponding time points in group S and group I∕R, respectively. The animals were sacrificed at 24 h of reperfusion and brains were removed to determine the brain water content, Evans blue ( EB) content and expression of occludin protein in cerebral cortex ( by Western blot) and to observe the ultrastructure of blood-brain barrier. Results Compared with group S, the brain water content and EB content were significantly increased, the expression of occludin protein was down-regulated (P＜0. 05), and the injury to ultrastructure of blood-brain barrier was accentuated in I∕R and Q groups. Compared with group I∕R, the brain water content and EB content were significantly de-creased, the expression of occludin protein was up-regulated (P＜0. 05), and the injury to ultrastructure of blood-brain barrier was significantly attenuated in group Q. Conclusion Quercetin pretreatment can de-crease the permeability of blood-brain barrier and attenuate brain edema, and the mechanism may be related to up-regulated expression of occludin protein in a rat model of global cerebral I∕R.
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Objective@#To investigate the cognition and intension of the enterostomal therapists for multi-sited practice, and explore the feasibility of the multi-sited practice among specialist nurses.@*Methods@#A questionnaire was developed and distributed in November 2017 to nurses qualified for enterostomal therapists and engaged in this work. 89.57% of the questionnaires were effectively recovered.@*Results@#The scorings of both the feasibility (3.78±0.97) and compliances (3.99±1.00) for enterostomal therapists to practice at multiple sites were higher than that (3.61±1.31) for feasibility of multi-sited practice of nurses at large. Around 95% of the respondents held that they could independently practice at multiple sites as enterostomal therapists, and two thirds of them proposed the regulatory authority for nurses′ multi-sited practice to be all the medical institutions or regional healthcare authorities which permit multi-sited practice of enterostomal therapists.@*Conclusions@#Specialist nurses represented by enterostomal therapists highly embrace nurses′ multi-sited practice, take a positive attitude towards their competence in this regard, and expect more stakeholders involved in setting up such a management system.
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The family doctor system is a collection of the rules and operating patterns formed during the interaction between the top design of "universal health coverage" and the "contractual experiment" at primary level. Its optimization and upgrading call for continuous attention to primary policy response. A questionnaire survey was made to medical workers at primary healthcare institutions in Zhejiang,to learn the comments and willingness of participation of family doctors for the contractual service policy. The survey found the poor policy response roots in such constraints as lack of effective connection between top level and primary level,poor incentive design,and delayed supporting policies. In view of upgrading supplier policy response,the authors recommended feasible strategies to optimize policy response, namely priori decision-making,process control,both hard and soft tactics,and parallel efforts for both internal and external sides.
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Objective: To review the surgical treatment progress in repair and reconstruction of acquired auricle defects. Methods: The related literature concerning the surgical methods and techniques for acquired auricle defects was reviewed and summarized. Results: In order to attain an aesthetic ear with a clear structure, the location, size, and condition of surrounding skin must be taken into account when planning excision and repair. The application of tissue engineering and digital technology for acquired auricle defects can achieve a satisfactory effectiveness. Conclusion: The surgical programs for acquired auricular defects have been constantly improved in recent years, and the emerging medical technologies also play a promoting role in the process, which providing a great deal of reference for obtaining structurally clear and stereoscopic auricle.
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<p><b>OBJECTIVE</b>To investigate the effects of different doses of propofol on pulmonary metastasis of intravenous injected MADB106 tumor cells and the expression of E-cadherin and β-catenin in the metastatic tumor tissue in rats.</p><p><b>METHODS</b>Forty Fischer 344 male rats were randomly divided into 4 groups (n=10) for intravenous administration of normal saline, intralipid, or propofol at 30 or 50 mg/kg via the femoral vein. One hour after the infusion, MADB106 tumor cells (2×10(5)) were injected intravenously in the rats. Three weeks later, pulmonary metastasis tumor foci and metastatic inhibitory rate were observed and the expression of E-cadherin and β-catenin in the metastatic tumor tissue were detected by immunohistochemistry.</p><p><b>RESULTS</b>Compared with the normal saline group, intralipid group showed no significant differences in the number of metastatic tumor foci in the lungs or E-cadherin and β-catenin expressions (P>0.05), which were all significantly lowered in the two propofol groups (P<0.05 or 0.01). The dose of propofol was inversely correlated with the number of metastasis tumor foci (r=-0.879) and expressions of E-cadherin (r=-0.755) and β-catenin (r=-0.693) (P<0.01).</p><p><b>CONCLUSION</b>Propofol can dose-dependently suppress pulmonary metastasis of intravenous injected MADB106 tumor cells by inhibiting the Wnt/β-catenin pathway and down-regulating E-cadherin and β-catenin expressions in the metastatic tumor tissue.</p>
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Animals , Male , Rats , Cadherins , Metabolism , Dose-Response Relationship, Drug , Down-Regulation , Immunohistochemistry , Injections, Intravenous , Lung Neoplasms , Drug Therapy , Neoplasm Metastasis , Drug Therapy , Neoplasm Transplantation , Propofol , Pharmacology , Rats, Inbred F344 , beta Catenin , MetabolismABSTRACT
Objective To evaluate the effects of dexmedetomidine on the oxidative stress responses during global cerebral ischemia-reperfusion (I/R) in rats.Methods Thirty-six male Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 3 groups (n =12 each) using a random number table:sham operation group (group S),global cerebral I/R group (group I/R) and dexmedetomidine group (group D).Global cerebral ischemia was induced by occlusion of bilateral common carotid arteries combined with hypotension (MAP maintained at 35-45 mmHg).In group D,dexmedetomidine was infused at a rate of 3 μg · kg-1 · h-1until 2 h of reperfusion after a loading dose of dexmedetomidine 3 μg/kg was intravenously injected immediately after onset of reperfusion.The neurological deficit score (NDS) was assessed at 24 h of reperfusion,the rats were then sacrificed,and their brains were immediately removed for determination of cell apoptosis and levels of malondialdehyde (MDA),superoxide dismutase (SOD) and catalase (CAT).Apoptotic rate was calculated.Results Compared with group S,NDS,apoptotic rate and MDA level were significantly increased,and SOD and CAT levels were decreased in I/R and D groups.Compared with group I/R,NDS,apoptotic rate and MDA level were significantly decreased,and SOD and CAT levels were increased in group D.Conclusion Dexmedetomidine attenuates global cerebral I/R injury through inhibiting the oxidative stress responses.
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Objective To evaluate the influence and safety of topical ketamine on postoperative sore throat following endotracheal intubation. Methods The clinical literatures concerning topical application of ketamine for the prevention of postoperative sore throat (POST) were searched from online databases. Randomized controlled trials were selected by the inclusive and exclusive criteria. Meta-analysis was conducted to assess the risk ratio(RR) of the incidence of POST and software Stata 12.0 was used in this analysis. Results Seven randomized trials involving 490 patients were included in this meta-analysis. The results of meta-analysis showed that the incidence of POST was significantly reduced in the ketamine group,with RR 0.61(95%CI 0.47~0.79,P<0.001) at 0~1 h,0.55(95%CI 0.43~0.71, P<0.001) at 4 h and 0.48 (95%CI 0.34 to 0.66, P<0.001) at 24 h after surgery. No major complications related to topical ketamine were observed. Conclusions For the patients receiving general anesthesia and endotracheal intubation, topical prophylactic application of ketamine can significantly reduce the incidence of POST without major complications.
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Objective To evaluate the effects of dexmedetomidine on the permeability of blood-brain barrier in rats subjected to global cerebral ischemia-reperfusion (I/R).Methods Thirty-six male Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 3 groups (n =12 each):sham operation group (group S),global cerebral I/R group (group I/R) and dexmedetomidine group (group D).Global cerebral I/R was induced by occlusion of bilateral common carotid arteries combined with hypotension (MAP was maintained at 35-45 mm Hg) in anesthetized rats.In group D,dexmedetomidine was infused at a rate of 3μg· kg-1 · h-1 until 2 h of reperfusion after a loading dose of dexmedetomidine 3 μg/kg was injected intravenously immediately after onset of I/R.The rats were sacrificed at 24 h of reperfusion and their brains were immediately removed for microscopic examination of hippocampal CA1 region and for determination of the cell apoptosis,brain water content,Evans blue content and aquaporin 4 (AQP4) expression.Results The number of apoptotic cells was significantly larger,and brain water content,Evans blue content and AQP4 expression were higher in groups I/R and D than in group S (P ＜ 0.05 or 0.01).The number of apoptotic cells was significantly smaller,and brain water content,and Evans blue content and AQP4 expression were lower in group D than in group I/R (P ＜ 0.05 or 0.01).Global cerebral I/R-induced pathological changes were significantly attenuated in group D.Conclusion Dexmedetomidine can decrease the permeability of blood-brain barrier and attenuate global cerebral I/R injury in rats,and down-regulation of AQP4 expression may be involved in the mechanism.
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Objective To investigate the effects of dexmedetomidine on global cerebral ischemia-reperfusion (I/R) injury in rats.Methods Fifty-four adult male SD rats weighing 200-250 g were randomly divided into 3 groups (n =18 each): shame operation group (group S),global cerebral I/R group (group I/R) and dexmedetomidine group (group D).Global cerebral I/R was produced by occlusion of bilateral common carotid arteries combined with hypotension (MAP maintained at 35-45 mm Hg).In group D dexmedetomidine 3 μg/kg was injected iv immediately after I/R,followed by infusion of dexmedetomidine at a rate of 3 μg· kg- 1 · h- 1 until 2 h of reperfusion.The neurological deficit score (NDS) was assessed (0 =normal,100 =brain death) at 6 h (T1),24 h (T2)and 72 h (T3) of reperfusion.Then six rats were sacrificed in each group and brain tissues were removed for microscopic examination of hippocampus CA1 region and determination of activity of myeloperoxidase (MPO),contents of TNF-α and IL-1β and expression of glial fibrillary acidic protein ( GFAP).Results Compared with group S,NDS,MPO activity and the contents of TNF-α and IL-1β at T1-3 were significantly increased,the expression of GFAP was up-regulated at T2,3 in groups I/R and D ( P ＜ 0.05 or 0.01).Compared with group I/R,NDS,MPO activity and TNF-α concent were significantly decreased at T1-3,IL-1β concent was decreased at T1,2,the expression of GFAP was down-regulated at T2,3 in group D (P ＜ 0.05 or 0.01 ).The pathologic changes were significantly attenuated in group D as compared with group I/R.Conclusion Dexmedetomidine can attenuate global cerebral I/R injury in rats,and the inhibition of inflammatory response may be involved in the mechanism.
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Objective To investigate the effects of lipoxin A4 (LXA4) on the inflammatory response to focal cerebral ischemia-reperfusion(I/R) inmy in rats.Methods Fifty-six healthy male SD rats weighing 200-250 g were randomly divided into 3 groups:group Ⅰ sham operation(group S,n=8);group Ⅱ cerebral I/R(n=24)and group Ⅲ lipoxin A4+I/R(group LXA4,n=24).Right mid-cerebral artery was occluded for 2 h by inserting cranially a nylon thread with rounded tip into internal carotid artery.LXA4 0.03 nmol/5 μl was injected into cerebral ventricle at 5 min after cerebral ischemia.Neurological deficit was scored at 24 h of reperfusion.Then four animals in each group were killed and their brains were removed for microscopic examination and expression of MPO at 24 h of reperfusion.Meantime,content of IL-1β,TNF-α,TGF-β1,and IL-10 in the brain tissue were measured at 1,6,12,24 and 48 h of reperfusion by ELISA.Glial cell activity was examined at 24 h of reperfusion by immuno-histochemistry.Results Intra-cerebroventricular administrated LXA4 0.03 nmol/5 μl provided mild neuroprotection against focal cerebral I/R injury,improved neurological deficits,and reduced morphological brain damages and PMN infiltration.LXA4 also decreased the content of TNF-α and IL-1β,and increased the content of IL-10 and TGF-β1.The numbers of activated astroglia and microglia were decreased in group LXA4 compared with group I/R.Conclusion LXA4 protects the brain against I/R injury by inhibiting inflammatory response.
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Objective To investigate the effect of lipoxin A4 ( LXA4 ) on the permeability of blood-brain barrier (BBB) after focal cerebral ischemia-repeffnsion (I/R) in rats. Methods Fifty-four adult male SD rats weighing 200-250 g were randomly divided into 3 groups ( n = 18 each): group Ⅰ sham operation (group S); group Ⅱ focal cerebral I/R ( group I/R) and group Ⅲ LXA4 ( group L). Focal cerebral I/R was produced by middle cerebral artery occlusion (MCAO) with a 4-0 nylon thread with rounded tip inserted into right internal jugular vein and threaded cranially in group Ⅱ and Ⅲ . In group Ⅲ LXA4 100 ng was injected into right lateral ventricle of the brain after MCA was successfully occluded. MCAO was maintained for 2 h. The neurological deficit was evaluated and scored (0 = no deficit, 5 = death) at 24 h of reperfusion. 2% Evans blue 4 ml/kg was injected via femoral vein at 1 h before the animals were sacrificed. The animals were killed and their brains were immediately removed for determination of brain water content, Evans blue content and expression of matrix metalloproteinase-9 (MMP-9)in the ischemic cortex. Results The neurologic deficit scores, the brain water and Evans blue content and MMP-9 protein expression in the cortex were significantly higher in I/R group than in S group. The cerebral I/R-induced changes were significantly attenuated in LXA4 group. Conclusion LXA4 can protect blood-brain barrier against cerebral I/R injury by inhibiting MMP-9 protein expression in the brain tissue.