Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 3 de 3
Filter
Add filters








Year range
1.
Medical Journal of Chinese People's Liberation Army ; (12): 1066-1071, 2017.
Article in Chinese | WPRIM | ID: wpr-694059

ABSTRACT

Objective To observe the changes of microglia in diabetic cerebral ischemia and reperfusion,and further explore the role of microglia in diabetic rats with cerebral ischemic injury.Methods Eighty healthy male SD rats were randomly divided into 4 groups:normal blood glucose sham operation group (NG sham group,n=5),diabetic hyperglycemia sham operation group (HG sham group,n=5),normal blood glucose with cerebral ischemia-reperfusion group (NG MCAO group,n=35) and diabetic hyperglycemia with cerebral ischemia-reperfusion group [HG middle cerebral artery occlusion (MCAO) group,n=35].The diabetic rats models were established by intraperitoneal injection of streptozotocin (STZ).The cerebral ischemia reperfusion models were made with MCAO,the specific marker protein Iba-1 was used to immunohistochemically label the microglia.The changes of microglia in the periventricular zone and caudate putamen region of the rats in HG MCAO group and NG MCAO group were observed at ischemia 30min and reperfusion 30min,3h,6h,Id,3d,7d and 14d (each time point contains 5 rats).Iba-1 and proliferating cell nuclear antigen (PCNA) immunofluorescence double labeling method were performed to detect the proliferation of microglia.Results After ischemia-reperfusion,the brain tissue appeared as obvious edema,mesh-like,HE staining faded,neurons swelled,cytoplasm vacuolization,nuclear pyknosis,and inflammatory cell infiltration.All these symptoms of brain injury were more obvious in HG group than in NG group.On the 3rd day after ischemia reperfusion,microglial cells were markedly activated in the infarct peripheral zone,piriform cortex and somatic sensory cortex,the activation reached the peak value at the 7th day,and the activated state continued to the 14th day of reperfusion.It was found with Iba-1 and PCNA immunofluorescence double labeling that,after cerebral ischemia-reperfusion,the increase of microglia number was related to its proliferation.The microglia proliferation also increased at the 3rd day after ischemia-reperfusion,and reached the peak value at the 7th day.The degree of microglia activation and proliferation was weaker in NG group than in HG group (P<0.05),but higher obviously when compared with their each sham group (P<0.05).Conclusion Hyperglycemia induced ischemia brain tissue microglia activation and proliferation inhibition may be involved in the hyperglycemia induced ischemic brain damage.

2.
Asian Pacific Journal of Tropical Medicine ; (12): 390-393, 2014.
Article in English | WPRIM | ID: wpr-819664

ABSTRACT

OBJECTIVE@#To observe the preventive and control effect of matrine on transforming growth factor (TGF-β1) and hepatocyte growth factor (HGF) of liver fibrosis tissue in rats.@*METHODS@#A total of 48 SD rats were randomly divided into A, B, C, D groups with 12 in each, group A as the normal control group and groups B, C, D as liver fibrosis models using composite modulus method with carbon tetrachloride (CCL4). Group B was the model group, group C adopted γ-interferon lavage therapy in the second day of modeling, and group D adopted matrine lavage treatment, at 4 and 8 weeks after treatment. Six rats were executed for detection of TGF-β1 and HGF, liver tissue histology and comparison fibrosis degree changes of rat liver tissue between groups.@*RESULTS@#Groups B, C, D showed a more significantly increased TGF-β1 at each time point compared with group A (P<0.05); Group B showed a more significantly increased TGF-β1 than groups C and D at weeks 4 and 8 (P<0.05); group D showed a lowest level of TGF-β1, followed by groups C and B. HGF of group B decreased more significantly than A group at weeks 4 and 8 (P<0.05); HGF of groups C and D was significantly elevated at 4 and 8 weeks than groups A and B (P<0.05), in which the group D showed the highest level of HGF. According to tissue histologic observation, rat liver tissue structure of group A was clear and normal, tissue structure of group B was destroyed with obvious fibrous tissue hyperplasia and fatty change of hepatic cells; groups C and D showed a slighter liver tissue damage, cell necrosis and connective tissue hyperplasia in collect abbacy than group B with a trend of obvious improvement.@*CONCLUSIONS@#Matrine can reduce TGF-β1 expression and enhance the activity of HGF, so as to realize the inhibition effect on liver fibrosis in rats.


Subject(s)
Animals , Male , Rats , Alkaloids , Pharmacology , Gene Expression , Hepatocyte Growth Factor , Genetics , Metabolism , Liver , Chemistry , Metabolism , Pathology , Liver Cirrhosis , Metabolism , Pathology , Protective Agents , Pharmacology , Quinolizines , Pharmacology , RNA, Messenger , Genetics , Metabolism , Rats, Sprague-Dawley , Transforming Growth Factor beta1 , Genetics , Metabolism
3.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 424-427, 2005.
Article in Chinese | WPRIM | ID: wpr-285854

ABSTRACT

<p><b>OBJECTIVE</b>To determine the threshold of millimeter wave irradiation for fetal injury in mice and the mechanism of decrease of learning and memory function in their offsprings and to verify whether the millimeter wave has the non-thermal effect.</p><p><b>METHODS</b>Pregnant mice were irradiated by millimeter wave with frequencies of 37.4, 42.2, 53.0 and 60.0 GHz at power densities of 1, 3, 5, 8 mW/cm(2) for two hours daily from the 6th to 15th day of their gestation. Learning and memory functions of their offsprings were tested by a Y-type electric maze. c-Fos protein expression level in hippocampus of their offsprings was determined with immunohistochemistry 0, 30, 60, 90 and 120 minutes after the offsprings were trained respectively.</p><p><b>RESULTS</b>The minimal power density of millimeter wave for the decrease in learning and memory function and decrease of c-Fos protein expression level in hippocampus of their offsprings caused by 37.4, 42.2 GHz and 53.0, 60.0 GHz was 5 and 3 mW/cm(2). Severity of injury for learning and memory in offsprings caused by irradiation increased with the power density of millimeter wave. The millimeter wave did not cause increase of the body temperature of the pregnant mice.</p><p><b>CONCLUSION</b>The threshold of millimeter wave with 37.4, 42.2 GHz, and 53.0, 60.0 GHz causing fetal injury in mice is 5 and 3 mW/cm(2) respectively. The decrease in learning and memory functions in offspring mice is related with decrease of c-Fos protein expression level in hippocampus. Millimeter wave has the non-thermal effects.</p>


Subject(s)
Animals , Female , Mice , Pregnancy , Dose-Response Relationship, Radiation , Hippocampus , Metabolism , Radiation Effects , Immunohistochemistry , Learning , Radiation Effects , Memory , Radiation Effects , Mice, Inbred BALB C , Microwaves , Prenatal Exposure Delayed Effects , Proto-Oncogene Proteins c-fos
SELECTION OF CITATIONS
SEARCH DETAIL