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To explore the feasibility of applying magnetic stimulation technology to the movement control of animal robots, the influence of coil radius, number of turns and other factors on the intensity, depth and focus of magnetic stimulation was simulated and analyzed for robot pigeons. The coil design scheme was proposed. The coil was placed on the head and one of the legs of the pigeon, and the leg electromyography (EMG) was recorded when magnetic stimulation was performed. Results showed that the EMG was significantly strengthened during magnetic stimulation. With the reduction of the output frequency of the magnetic stimulation system, the output current was increased and the EMG was enhanced accordingly. Compared with the brain magnetic stimulation, sciatic nerve stimulation produced a more significant EMG enhancement response. This indicated that the magnetic stimulation system could effectively modulate the functions of brain and peripheral nerves by driving the coil. This study provides theoretical and experimental guidance for the subsequent optimization and improvement of practical coils, and lays a preliminary theoretical and experimental foundation for the implementation of magnetic stimulation motion control of animal robots.
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Animals , Columbidae , Robotics , Motion , Brain , Magnetic PhenomenaABSTRACT
Curriculum integration has become the core content of the current medical education reform.With the rapid development of information technology,how to reflect the teaching and learning effects and to further improve them,is one of the difficulties in the reform of the integrated curriculum.In view of the problems of single form of assessment model,separate classroom teaching and extracurricular teaching evaluation,low utilization of network and electronic teaching resources,we make full use of network methods to carry out reform on the current formative teaching evaluation system.With the purpose of formative assessment and evaluation,the "Blackboard network teaching system" of the curriculum has been built,and the evaluation indexes of classroom teaching and extracurricular teaching have been established.And at the same time,the formative assessment index has been enriched and perfected in a diversified form,and the formative assessment model adapted to the integrated curriculum is preliminarily explored.
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Objective@#To evaluate the safety and feasibility of treating de novo coronary lesions with paclitaxel-eluting balloon.@*Methods@#This is a retrospective study, which enrolled 76 patients with 80 de novo coronary lesions treated with paclitaxel-eluting balloons(<30% residual stenosis and there was no blood flow limited dissection after pretreatment) from April 2015 to November 2016 in Guangdong general hospital. The data of basic characteristics,procedures,devices and follow-up information were retrieved and analyzed. The primary endpoint was the composite of cardiac death, recurrent myocardial infarction and target lesion revascularization.@*Results@#(1)The age was (63.3±10.3) years. There were 68.4%(52/76) acute coronary syndrome patients, prevalence of type 2 diabetes was 36.8%(28/76), and 64.5%(49/76)patients with at least one high bleeding risk. (2)The lesion length was (17.4±7.6)mm, and the stenosis was (88.1±8.2)%.The reference vessel diameter≥2.75 mm accounted for 51.2% (41/80), and bifurcation stenosis accounted for 67.5%(54/80). (3)53.7%(43/80) lesions were pretreated with scoring balloon to optimize plaque modification. The paclitaxel-eluting balloon length and diameter were (22.3±5.5)mm and (2.74±0.52)mm.The residual stenosis was (12.3±10.3)%. Procedural success was 88.8%(71/80).Bail-out stenting rate was 5.0%(4/80). (4)The median follow-up duration was 12(6, 25) months. Primary endpoint occurred in 3 cases (3.9%), including 2 cardiac deaths(1 patient died of recurrent myocardial infarction, and 1 patient died of acute heart failure induced by severe mitral insufficiency), and one patient receivedtarget lesion revascularization.@*Conclusion@#In case of no more than 30% residual stenosis and no blood flow limited dissection after lesion pretreatment,it is safe and feasible to treat de novo coronary lesionsusing paclitaxel-eluting balloon.
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Aim To explore the effect of meloxicam on the CUMS-induced depressive-like behaviors in rats and its preliminary mechanism. Methods The rats were exposed to CUMS procedure for 6 weeks to estab-lish the model of depression. Meloxicam(1,3 mg· kg-1 ) and sertraline(5 mg·kg-1 ) were administered to rats from 22d of the stress procedure(once a day,for 21 days,p. o. ) . Depressive-like behaviors were evalu-ated by the open-field test and force swimming test. The levels of PGE2 and TNF-αin cortex were measured by ELISA. Moreover, the concentrations of NE, DA, DOPAC and 5-HIAA were also measured by HPLC, and the protein expression of 5-HT1 AR in cortex was analyzed by the immunohistochemistry. Results Com-pared with the rats of normal control group,the vertical and horizontal movement scores of rats in the open-field test were decreased and the immobility time in the forced swimming test was increased in model group. The levels of PGE2 and TNF-α were both increased signifi-cantly,whereas the concentrations of NE, DA, DOPAC and 5-HIAA were decreased and the expression of 5-HT1AR was reduced in cortex. Compared with the rats of model group, meloxicam significantly improved the depressive behaviors of rats in experimental groups and reversed the content of PGE2 ,TNF-α,NE,DA,DOPAC and 5-HIAA, as well as the expression of 5-HT1AR. Conclusion Meloxicam has a significant protective effect on CUMS-induced depressive-like behaviors, and the protective mechanism might be related to atten-uating inflammation response and reconstructing the balance of the monoamine neurotransmitter system in rat cortex.
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<p><b>OBJECTIVE</b>To observe the long-term relationship between body mass index (BMI) and cardiovascular events in male elderly hypertensive patients.</p><p><b>METHODS</b>A total of 839 male elderly (>65 years old) hypertensive patients were included in this prospective study. Baseline data were obtained on January 2004 and participants were followed up yearly till January 2014. Patients were divided into 3 groups according to their BMI: normal weight group (18.5 kg/m² ≤ BMI<24.0 kg/²), overweight group (24.0 kg/m² ≤ BMI<28.0 kg/m²), obese group (BMI ≥ 28.0 kg/m²). All-cause death and cardiovascular events were compared.</p><p><b>RESULTS</b>The average age of all 839 hypertension men was (75.4 ± 4.8) years at baseline. Baseline systolic blood pressure was (133.7 ± 14.6) mmHg (1 mmHg=0.133 kPa), diastolic blood pressure was (74.3 ± 9.3)mmHg. Baseline systolic and diastolic blood pressure was similar among the three groups. All 839 patients completed follow-up. There were 178 all-cause deaths, 54 cardiovascular deaths, 51 new/recurrent myocardial infarctions and 105 new/recurrent strokes during follow up. Incidence of all-cause mortality in overweight group (16.74%,72/430) was significantly lower than in normal weight group (27.01% (74/274), P<0.05). Kaplan-Meier curves showed the all-cause mortality and cardiovascular mortality were higher in normal weight group than in the other two groups. According to the Cox proportional hazards regression model, the risk of all-cause mortality (RR=0.867, 95% CI: 0.792-0.949) and cardiovascular death (RR=0.179, 95% CI : 0.05-0.645) in patients with a BMI ≥ 24.0 kg/m² were lower than in the group with BMI<24.0 kg/m².</p><p><b>CONCLUSION</b>Obesity paradox phenomenon is observed in elderly male hypertensive patients in that higher BMI is associated with lower mortality risks in elderly male hypertensive patients during the 10 years follow-up.</p>
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Aged , Humans , Male , Blood Pressure , Body Mass Index , Cardiovascular Diseases , Cause of Death , Hypertension , Incidence , Overweight , Proportional Hazards Models , Prospective StudiesABSTRACT
Aim To investigate the effects of baicalin on cognitive function in global cerebral ischemia reper-fusion rats, and the probable mechanism involved. Methods Sixty male Sprague-Dawley(SD) rats were randomly divided into Sham operation group ( S group) , global cerebral ischemia reperfusion group ( I/R group) , global cerebral ischemia reperfusion + ba-icalin treatment group ( I/RB group) , twenty in each. Model was induced via the bilateral occlusion of the common carotid arteries plus hemorrhagic hypotension. 12 h after reperfusion, rats in I/RB group were given baicalin (100 mg·kg-1 ) saline solution by intragas-tric administration twice per day for 7 days. Rats in S group and I/R group were given the corresponding dose of saline infusion at the same time. Morris water maze test was employed to detect spatial learning and memo-ry. BrdU immunohistochemistry was used to detect the proliferation of neural precursor cells ( NPCs ) in the brain. Expression of COX-2 in the brain tissue was measured by Western blot. Results Compared to I/R group, baicalin improved spatial learning and memory damage ( P nitive function in the rats with global cerebral ischemia reperfusion, which might be associated with its inhibi-tory effects on the expression of COX-2 , thereby in-creasing the proliferation of NPCs in the brain.
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Aim To establish primary cultured rat hip-pocampal neuron damage model induced by aluminum maltolate and study the effect of intervention for DP2 on primary cultured rat hippocampal neuron treated with aluminum overload. Methods The hippocampus was dissected out from fetal rat ( embryonic 18 d ) . After being cultured for 7 d, the hippocampal neuron was treated with Al( malt) 3 to establish the model of prima-ry cultured rat hippocampal neuron damage and mean-while treated with DP2 agonist DK-PGD2 and DP2 an-tagonist CAY10471, respectively. After treatment for 24 h, the cell viability was measured by MTT and LDH, Ca2+ fluorescence intensity. Neuronal pathomor-phology was observed by HE staining. Results The purity of hippocampal neuron was more than 95%. Compared with the control group, the number of hipp-ocampal neurons was reduced and neurons became chromatic agglutination and karyopyknosis in aluminum overload group. Treatment of aluminum caused a sig-nificant decrease in MTT value ( P<0. 01 ) and an in-crease in the LDH leakage rate (P<0. 01). The Ca2+fluorescence intensity significantly increased ( P <0. 01 ) in aluminum overload group. Compared with that of the aluminum overload group, treatment of DK-PGD2 , a selective DP2 agonist, significantly aggravated the primary cultured rat hippocampal neuron injury caused by aluminum overload accompanied with the significant decrease of MTT value ( P <0. 01 , P <0. 05 ) and an increase of the LDH leakage rate ( P<0. 01), significant increase of Ca2+ fluorescence inten-sity of neuron. Treatment of CAY10471, a selective DP2 antagonist, had opposite effects of DK-PGD2 . Conclusion The activation of DP2 can increase hipp-ocampal neural susceptibility to aluminum overload.
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Objective To explore the application of optical coherence tomography in vascular tissue engineering culture by dynamic monitoring its changes.Methods Human umbilical artery smooth muscle cells were isolated and culture by tissue block method.After passage culture and cell surface markers evaluation, smooth muscle cells were seeded onto polyglycolic acid scaffold and placed into the bioreactor based on Luo-Ye pump with pulsatile stress for three-dimensional culture.At 1、4、 7 、10、14、17、21 days in culture, the image data was obtained by optical coherence tomography technology.The ability of imaging TEBV via OCT was analyzed combined with histopathological observation.Results As the incubation time extended,OCT clearly showed PGA gradual degradation, decreased composite scaffold thickness and the wall structure from loose to tight.At 21 days in culture, the vessel mimics had smooth surface with extracellular matrix evenly distributed and achieved complete reconstruction in the PGA scaffold.Combining with histopathological staining, the blood vessel mimics were similar to natural blood vessels.OCT measured TEBV thickness compared with histopathological measurement had good correlation (r =0.922,P ＜ 0.05).Conclusion Optical coherence tomography could clearly image microstructures of tissue engineered blood vessels cultured in three-dimensional culture system based on Luo-Ye pump, delineate the reconstruction of TEBV-like tissue in the bioreactor and provide as a dynamic and convenient monitoring tool in vascular tissue engineering.
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Objective: To explore the predictive value of fractional lfow reserve (FFR) level for long-term prognosis in patients after coronary drug-eluting stent (DES) implantation, and to analyze the relevant factors affecting the level of post-operative FFR. Methods: A total of 135 patients who received DES implantation in our hospital from 2012-01 to 2013-07 with coronary intermediate lesion at (50-80) % were studied. The relevant factors for MACE occurrence were studied by multivariate logistic regression analysis, the post-stent FFR level for predicting the long term prognosis after DES implantation was ifnally analyzed by ROC curve. Results: All patients ifnished 1 year follow-up study including 104 male and 31 female with the mean age of (63 ± 9) years. The post-stent FFR level was lower in MACE group than that in Non-MACE group, (0.82 ± 0.07) vs (0.87 ± 0.06),P=0.004. Multivariate logistic regression analysis presented that the higher level of post-stent FFR was the protective factor for MACE occurrence (OR=0.212,P=0.039); the post-stent FFR level had certain predictive value for MACE occurrence at 1 year after DES implantation (AUC=0.706,P=0.006); Kaplan-Meier survival study showed that the patients with post-stent FFR<0.875 had the less MACE occurrence than those with FFR≥0.875,P=0.012. Multivariate logistic regression analysis also indicated that post-stent FFR≥0.875 was positively related to right coronary target vessel, higher pre-operative FFR level and larger stent diameter.Conclusion: Post-stent FFR level had certain predictive value for MACE occurrence in patients at 1 year after DES implantation, the patients with post-stent FFR≥0.875 had the lower MACE occurrence rate than those with FFR<0.875.
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<p><b>OBJECTIVE</b>To study the relationship between carbon dioxide combining power(CO₂-CP) and contrast-induced acute kidney injury (CI-AKI) in patients with ST segment elevation myocardial infarction and undergoing percutaneous coronary intervention.</p><p><b>METHODS</b>We retrospectively analyzed 174 patients admitted to our hospital from March 2012 to August 2013 with ST segment elevation myocardial infarction and underwent emergency percutaneous coronary intervention. Patients were divided into three tertiles according to pre-operative CO₂-CP: T1 (CO₂-CP < 22.62 mmol/L), T2(CO₂-CP 22.62-24.30 mmol/L), T3(CO₂-CP > 24.30 mmol/L). Baseline clinical data, CI-AKI incidence, in-hospital mortality and dialysis rate were compared among groups. An increase in serum creatinine of >26.4 µmol/L and/or >50% from baseline within 48 hours after contrast exposure was defined as CI-AKI. Univariate logistic regression analysis was used to identify the risk factors of CI-AKI. The relationship between CO₂-CP and CI-AKI was assessed by multivariate logistic regression analysis. Receiver operating characteristic curve was used to identify the optimal cutoff of the CO₂-CP for predicting CI-AKI.</p><p><b>RESULTS</b>CI-AKI occurred in 25 (14.4%) patients, and lower CO₂-CP was related to higher incidence of CI-AKI (27.6% (16/58) in group T1, 5.3% (3/57) in group T2, 1.7 % (1/59) in group T3, P = 0.002) and higher in-hospital mortality (10.3% (6/58) vs. 0 and 1.7% (1/59), P = 0.010). Dialysis rate was similar among 3 groups (5.2% (3/58) vs. 0 and 1.7% (1/59), P = 0.168). The incidence of CI-AKI was significantly associated with CO₂-CP < 22.00 mmol/L in univariate analyses (OR = 6.767, 95% CI 2.731-16.768, P < 0.001). After adjusting for potential confounding risk factors, CO₂-CP < 22.00 mmol/L remained significantly associated with the incidence of CI-AKI (OR = 5.835, 95%CI 1.800-18.914, P = 0.003) in multivariate logistic regression. ROC analysis revealed that the optimal cutoff of CO₂-CP to predict CI-AKI was 22.00 mmol/L (sensitivity 64.0%, specificity 79.1%, AUC = 0.714).</p><p><b>CONCLUSIONS</b>Pre-percutaneous coronary intervention CO₂-CP in patients with ST segment elevation myocardial infarction undergoing percutaneous coronary intervention is related to CI-AKI. CO₂-CP < 22.00 mmol/L predicts higher risk of CI-AKI in this patient cohort.</p>
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Humans , Acute Kidney Injury , Carbon Dioxide , Contrast Media , Hospital Mortality , Incidence , Kidney , Logistic Models , Myocardial Infarction , Percutaneous Coronary Intervention , ROC Curve , Retrospective Studies , Risk FactorsABSTRACT
Aim To investigate the protective effects of beraprost sodium on cerebral cortical neuron injury in chronic aluminum-overload rats and its effects on PGIS-IP signaling pathway. Methods 75 SD rats were randomized into five groups: normal control group, chronic aluminum-overload group ( model group) and beraprost sodium groups-low dose (6 μg· kg-1 ), medium dose ( 12 μg · kg-1 ) and high dose (24 μg·kg-1). Aluminum gluconate (Al3+ 200 mg ·kg-1 d-1, once a day, 5d a week, for 20 weeks, p. o. ) was administered to rats of cerebral damage model. The rats of experimental groups were concomi-tantly treated with beraprost sodium ( p. o. ) daily for 20 weeks. After the model was built successfully, the spatial learning and memory( SLM) function was done by Morris water maze. The cortical neurons damage was detected by HE staining, SOD activities and MDA contents. The 6-k-PGF1α levels in cortex were meas-ured by ELISA. The expressions of PGIS, IP mRNA and IP protein were also studied. Results Compared with the rats of normal control group, the SLM function was significantly impaired ( P<0. 01 ) and considera-ble karyopycnosis was observed in model group rats. The SOD activities were weakened ( P <0. 01 ), the MDA contents increased ( P<0. 05 ) and the levels of 6-k-PGF1α raised significantly ( P <0. 01). The ex-pressions of PGIS and IP mRNA in the rats cortex obvi-ously increased ( P<0. 01 ), so did the expression of IP protein(P<0. 05). Compared with the rats of mod-el group, the SLM function of rats in experimental groups decreased significantly ( P<0. 01 ) and damage of cortical neurons reduced remarkably. The SOD ac-tivities increased ( P <0. 01 ) and the MDA contents decreased ( P <0. 01). Besides, the content of 6-k-PGF1α, the expressions of PGIS mRNA and IP protein in the rats cortex decreased significantly ( P<0. 05 ) as well as IP mRNA ( P<0. 01). Conclusion Our re-sults demonstrate that in cerebral cortical neuron of chronic aluminum-overload rats, beraprost sodium has notably protective effects and the mechanism might be related to PGIS-IP signaling pathway.
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Aim To investigate the effects and mecha-nism of nuclear factor-κ B inhibitor, PDTC, on global cerebral ischemia reperfusion ( GCIR ) rat hippocam-pus. Methods Forty-eight adult male Sprague-Daw-ley rats were randomly divided into one control group receiving sham operation and three experimental groups all receiving global cerebral ischemia for 20 min. In PDTC 100 mg·kg-1 group ( P100 ) and PDTC 200 mg ·kg-1 group ( P200 ) , PDTC 100 mg · kg-1 or PDTC 200 mg·kg-1 was injected ip one hour before ischemi-a respectively. Spatial learning and memory function of rats were tested using Morris water maze. HE staining was employed to observe pathological changes of hipp-ocampal neurons. Expression of COX2 was measured by Western blot, and the content of PGI2 and TXA2 in rat hippocampus was detected by enzyme-linked immu-nosorbent assay. Results A significant increase of es-cape latency was observed in GCIR group compared to the sham operation group(P<0.05). PDTC 100 mg· kg-1 and PDTC 200 mg · kg-1 significantly reduced escape latency ( P <0.05 ) and histopathological injury in CA1 region of hippocampus. PDTC 100 mg · kg-1 and PDTC 200 mg · kg-1 also reduced COX2 expres-sion, PGI2 content, TXA2 content and PGI2/TXA2 . Conclusion Pretreatment with PDTC can protect hip-pocampus from GCIR injury through inhibition of COX2 expression and PGI2/TXA2 .
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This study is to investigate the anti-tumor activities of a novel cyclophosphamide derivate 4, 6-diphenyl cyclophosphamide (9b) in vivo and in vitro, and its possible mechanism of action. The inhibitory effects of 9b on human hepatoma cell line HepG2, human breast carcinoma cell line MCF-7 and human myeloid leukemia cell line K562 were measured by MTT assay in vitro. Cell cycle distribution and apoptotic rate were evaluated by flow cytometry. To evaluate the anti-tumor effect of 9b in vivo, mouse model bearing inoculated H22 tumor was established. The results indicated that 9b could inhibit the proliferation of HepG2, MCF-7 and K562 cells in a dose and time dependent manner. The ICo50 values of 9b were 32.34 micromol.L-1 to HepG2 cells, 87.07 micromol.L-1 to MCF-7 cells and 149.10 micromol.L-1 to K562 cells after incubation for 48 h. The results of flow cytometry indicated that after being treated for 48 h with different concentrations of 9b, the ratios of HepG2, MCF-7 cells at the Go/G1 phase and K562 cells at the G0/Gl phase and G2/M phase increased significantly compared with control group, and the apoptotic rate increased with the increase of the concentration of 9b. 9b could significantly reduce tumor weight of H22 solid tumor mouse model in vivo. To summarize, 9b showed significantly anti-tumor activity in vivo and in vitro, of which the mechanism might be associated with the change of cell cycle distribution and induction of tumor cell apoptosis.
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ObjectiveTo investigate the effects of exercise on the hippocampal formation and the myelinated nerve fibers in the hippocampal formation of middle-aged rats. MethodsTen 14-month female SD rats were randomly divided into exercise group and sedentary group.Rats in the exercise group were forced to run on a treadmill for 4 months. After 4 months, spatial learning capacity of two group rats was tested using the Morris water maze.Then, the hippocampal formation and the myelinated nerve fibers in the hippocampal formation were quantitatively estimated using transmission electronic microscopy and stereological techniques. Results Treadmill running enhanced the spatial learning capacity of the rats. The volume of hippocampal formation and the total length of the myelinated nerve fibers in the hippocampal formation were significantly increased after 4 months exercise.However,there was no significant difference in the total volume of the myelinated fibers in the hippocampal formation between the two groups.The absolute distributions of the total length of the myelinated fibers in the hippocampal formation of two groups indicated that the exercise-induced increase of the total length of the myelinated nerve fibers in the hippocampal formation was mainly due to the increase of the myelinated fibers with small diameter. Conclusions Four months running exercise remarkably influence the spatial learning capacity,hippocampal formation and the myelinated fibers in the hippocampal formation of the middle-aged famale SD rats. The present results reveal a potential mechanism for the fact that exercise might improve brain function.
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ObjectiveTo investigate the effects of short-term enriched environment on the hippocampal formation and the myelinated fibers in the hippocampal formation of mid-aged male rats. MethodsTwenty 14-month old male SD rats were randomly divided into enriched group and standard group. Enriched rats were reared in enriched environment and standard rats were reared in standard environment for 4 months. Then, the spatial learning capacity of enriched rats and standard rats was tested with the Morris water maze. After the Morris water maze test, the total volume of the hippocampal formation and the myelinated nerve fibers in the hippocampal formation were quantitatively estimated with transmission electronic microscopy technique and stereological methods. Results There was not significant difference in the spatial learning capacity between enriched group and standard group. The total volume of the hippocampal formation of enriched rats was not significantly increased by 4.6% when compared with that of standard rats. The total volume, total length and mean diameter of the myelinated nerve fibers in the hippocampal formation of enriched rats were significantly increased when compared with those of standard rats. Conclusions Four-months enriched environment significantly affected the myelinated fibers in the hippocampal formation of mid-aged male SD rats. The present results might provide an important theoretical basis for searching the ethology strategy to delay the progress of brain aging in the future.
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ObjectiveTo investigate the effects of short-term enriched environment on the hippocampal formation and the myelinated fibers in the hippocampal formation of mid-aged female rats. Methods Twenty 14-month female SD rats were randomly divided into 10 enriched environment (EE) rats and 10 standard environment (SE) rats. EE rats were reared in enriched environment and SE rats were reared in standard environment for 4 months. Then, five rats were randomly selected from each group. The spatial learning capacity was assessed with Morris water maze. The hippocampal formation and the myelinated fibers in the rat hippocampal formation were quantitatively investigated with transmission electronic microscopy technique and stereological methods. Results Short-term enriched environment enhanced the spatial learning capacity of the mid-aged female rats. The total length and total volume of the myelinated fibers in the hippocampal formation of the EE rats was significantly increased by 43.3% and 47.4%, respectively, when compared to the SE rats. There was no significant difference in the hippocampal volume and the mean diameter of the myelinated fibers in the hippocampal formation between two groups. The increase of the total length of the myelinated nerve fibers in the hippocampal formation was mainly due to the increase of the myelinated fibers with small diameter. Conclusion Short-term enriched environment had significant effects on the spatial learning capacity and the myelinated fibers in the hippocampal formation of middle-aged female rats.
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Aim To investigate the effect of fenofibrate on focal cerebral ischemia injury in rats and its mechanism.Methods The rat model of global cerebral ischemia/reperfusion injury was established by bilateral common carotid arteries occlusion combined with hemorrhagic hypotension.Fenofibrate (33, 100, 300 mg·kg~(-1)) was intragastriclly administered 30 min before the operation, MK886 (6 mg·kg~(-1)) was given intraperitoneally 30 min before administration of fenofibrate (300 mg·kg~(-1)).Morris water maze was used to evaluate the ability of spatial learning and memory function.HE staining was used to observe pathological morphological changes of hippocampal neurons. NF-κBp65 expression was detected by immunohistochemistry, SOD activities and MDA contents were analyzed by biochemistry, and IL-1β, IL-6, IL-10, TNF-α levels were detected by ELISA.Results Fenofibrate remarkably improved the spatial learning and memory function, obviously prevented the hippocampal neurons from karyopycnosis and losing induced by I/R. Fenofibrate significantly blunted the increase of MDA, NF-κBp65, TNF-α, IL-1β, IL-6, and the decrease of IL-10 and SOD activities of I/R rats.Conclusions Fenofibrate has an obviously neuroprotective effect on global cerebral ischemia/reperfusion damage by activating PPARα.The anti-inflammation and antioxidative stress of fenofibrate may be involved in the protective mechanism.
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Aim In order to study the protective effect of caffeic acid on damage induced by aluminum-overload in primary cultured rat hippocampal neuron.Methods Primary cell cultures were obtained from the cerebral hippocampus of Newly born SD rats within 24 h.On the d 7 of neuronal culture, the immunohistory of NSE was used to identify the purity of neuron.There were 5 experimental groups,NaCl(200 μmol·L~(-1))-treated group, AlCl_3-treated group(200 μmol·L~(-1)),and aluminum+caffeic acid(10~(-6) mol·L~(-1),10~(-7) mol·L~(-1) and 10~(-8) mol·L~(-1))-treated groups. HE staining was used to observe the change of neuronal pathomorphology. The cell viability was measured by MTT assay. SOD activity, LDH leakage and MDA contents were also detected.Results The purity of neurons was more than 95%. Aluminum administration induced loss of neurons and damage to dendrite and axon.Compared with that of the control group,the decreased viability of neurons,increased leakage of LDH, decreased activity of SOD and increased contents of MDA were observed in aluminum-treated groups.Compared with that of the model group, the administration of Caffeic acid could significantly blunt the death of the primary cultured hippocampal neurons, and blunt the decrease of neuronal viability and SOD activity and the increase of LDH leakage and MDA contents.Conclusions These results suggest that caffeic acid has an obvious protective effect against neuronal damage induced by aluminum overload in primary cultured neurons. The mechanism of protection might involve the anti-inflammation and anti-oxidative effects of caffeic acid.
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<p><b>OBJECTIVE</b>To study the dose- and time-dependent protective effects and the synergistic effects of nimodipine (NMDP) and fructose-1,6-diphosphate (FDP) against cerebral damage induced by acute carbon monoxide (CO) poisoning in mice.</p><p><b>METHODS</b>Male mice were exposed to CO 170 mL/kg, i.p. After CO intraperitonealy exposure, mortality of mice, change in memory function estimated by passive avoidance test, the pathomorphologic observation of brain tissue slices, as well as changes of activities of monoamine oxidase (MAO)-B and Ca(2+)-Mg(2+)-ATPase in cerebral tissue were studied. In dose-dependent protective effect study, NMDP (10.6, 5.3, 2.7 mg/kg) and FDP (2.6, 1.3, 0.67 g/kg) was injected ip, respectively 15 min after CO exposure. To study the time-effect relationship of drugs, NMDP (5.3 mg/kg) and FDP (1.3 g/kg) were administered ip respectively 15 minutes, 45 minutes and 120 minutes after CO exposure. The combination of NMDP (2.7 mg/kg) and FDP (0.67 g/kg) was administered ip15 minutes, 45 min and 120 minutes after CO exposure to study the synergism of the two drugs.</p><p><b>RESULTS</b>Either NMDP (10.6, 5.3 mg/kg) or FDP (2.6, 1.3 g/kg) administered ip within 15 minutes after CO exposure significantly decreased the impairment of memory function and mortality rate induced by CO, inhibited the decrease of Ca(2+)-Mg(2+)-ATPase activity, blunted the rising of MAO-B activity and prevented the delayed hippocampal neuronal death in poisoning mice. To our surprise, the combined use of NMDP (2.7 mg/kg) and FDP (0.67 g/kg) within 15 minutes after CO exposure had similar effects to that in NMDP (10.6, 5.3 mg/kg) and FDP (2.6, 1.3 g/kg).</p><p><b>CONCLUSIONS</b>These results suggest that the impairment of CO on brain can be attenuated if NMDP or FDP are administered sufficiently and quickly as soon as possible after CO exposure and there exists a synergism of FDP and NMDP against CO poisoning damage.</p>
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Animals , Male , Mice , Brain Damage, Chronic , Calcium Channel Blockers , Therapeutic Uses , Carbon Monoxide Poisoning , Dose-Response Relationship, Drug , Drug Synergism , Fructosediphosphates , Therapeutic Uses , Neuroprotective Agents , Therapeutic Uses , Nimodipine , Therapeutic Uses , Time FactorsABSTRACT
Aim To investigate the effects of heme oxygenase-1(HO-1) on brain damage due to cerebral ischemia/reperfusion.Methods 120 male mice were divided into four groups randomly and the cerebral ischemia/reperfusion(I/R) model was established through drawing out and reperfusing 40% of the whole blood volume in combination with clamping the carotid arteries for 20 min after anesthesia with 40 g?L-1chloral hydrate(400 mg?kg-1 ip).The mice were intracerebraventricularly(icv) injected with 3(l of150 ?mol?L-1 hemin,150 ?mol?L-1 ZnPPIX,or artificial cerebrospinal fluid(ACSF),respectively 16 h before the model established.Sham operation group only received anesthesia and operation without I/R and icv injection.The hippocampal HO activity and cerebral cortex xanthine oxidase(XO) activity,the levels of malonaldehyde(MDA) and reactive oxygen species(ROS),hippocampal neuron apoptosis,and hippocampal HO-1 expression were determined by spectrophotometer,TUNEL method,and Western blot,respectively.Results The increased hippocampal HO-1 expression and HO activity,decreased XO activity,MDA and ROS levels,and diminished hippocampal apoptosis were observed in the hemin group,compared with ACSF group(P0.05),but inhibited the activity of HO with the elevation of XO activity,MDA and ROS levels,as well as cellular apoptosis(vs ACSF,P