The dynamic expression of Glial Fibrillary Acidic protein in peri-cerebral Hemorrhage of rat model
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Objective: The purpose of this research is to investigate the role of glial fibrillary acidic protein (GFAP) in intracerebral hemorrhage (ICH) of animals model.Methods:ICH rat model was made by stereotactic technology, and sham injections served as controls. We measured brain water content, and GFAP expression after ICH.Results: The measured results show that the brain edema achieves the peak value 48 hours after ICH. The brain edema is statistically significantly higher than that of the comparison group (P0.05). The number of the masculine cells with obvious GFAP immunity reaction around haematoma area was observed to achieve the highest at 6 hours and the lowest at 72 hour after ICH. Seven days after ICH, the quantity of masculine cells increased significantly comparing to that after 72 hours (P0.05) but less than the quantity after 6 hours (P0.05). The ICH group of those masculine cells with the comparison group at different times demonstrates the validation of this study method statistically (P0.05).Conclusion: The GFAP reactions in intracerebral hemorrhage area are highly related to brain edema, indicating that astrocyte plays a pivotal role in the pathological change of intracerebral hemorrhage. It either restrains or expedites the reparation of the intracerebral hemorrhage.Keywords:
Brain Edema
Rat model
Peri
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Objective: To study the expression of aquaporin4(AQP4) protein in perihematomal tissue after intracerebral hemorrhage(ICH) in rats. Methods: The experimental ICH m odel was established in rats by injecting quantitative collagenase into the left caudate nuclei of the rats. The changes of brain water content(BWC) were measur e d by the wet and dry weight methods. Immunohistochemistry was used to determine the change of expression of AQP4 protein during different periods after ICH. Results: BWC and AQP4 protein expression in perihematomal tissue were increased at 6 ho urs after ICH and reached peak at 72 hours. In one week following ICH, it was st il l higher than normal level. In addition, the expression of AQP4 was positively c orrelated with BWC(r=0 985 7,P0 01). Conclusion: AQP4 has a relevant relationship with the formation of brain edema after ICH.
Brain Edema
Brain tissue
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Objective:To study the effects of hyperbaric oxygen(HBO) on brain edema and expression of aquaporin-4(AQP-4) surrounding brain tissue of hemorrhagic focus following experimental intracerebral hemorrhage(ICH) in two kinds of rat models.Method:A total of 126 rats were randomly divided into five groups:sham-operated group(SHG,6 rats);control-1 group(autologous blood induced intracerebral hemorrhage model,A-ICH,30 rats),control-2 group(collagenase-induced intracerebral hemorrhage model,C-ICH,30 rats),trial-1 group(A-ICH+HBO,30 rats),trial-2 group(C-ICH+ HBO,30 rats).HBO therapy was intervened at 24h after operation,once a day.All rats were sacrificed at 24h,48h,72h,5d,7d post operation(each time point 6 rats).Brain edema and expression of AQP-4 were tested.Result:The success rates of A-ICH model and C-ICH model were 65% and 75% respectively.Brain edema content of A-ICH,C-ICH,A-ICH+HBO and C-ICH+HBO groups were significant higher than that of SHG group(P 0.05).The cerebral edema of A-ICH+HBO and C-ICH+HBO groups alleviated obviously compared with A-ICH and C-ICH groups,and the difference was significant respectively at 48h,72h,5d,7d and 48h,5d post operation(P 0.05).The brain edema of A-ICH+HBO group alleviated more early and obviously than that of C-ICH+HBO group,especially at 72h post operation(P0.05).The expression of AQP-4 appeared in all rats brain tissue,but expression of AQP-4 in SHG group was lower.That of A-ICH and C-ICH groups started rising at 24h post operation,the peak appeared at 48h,then dropped at 72h,but there were still significant different compared with SHG group at 7d post operation(P0.05).The difference between A-ICH group and C-ICH group was significant at 72h post operation(P0.05),and the difference between A-ICH+HBO group and A-ICH group was significant at all time points post operation(P0.05).but the difference between C-ICH+HBO group and C-ICH group was significant only at 48h and 72h post operation(P0.05).Compared with C-ICH +HBO group,expression of AQP-4 in A-ICH+HBO group was more obvious and early,especially at 48h and 72h post operation(P0.05).Conclusion:HBO might play neuroprotection role by relieving brain edema and down-regulating AQP-4 expression.A-ICH model was more fit for brain edema study of ICH rat.
Brain Edema
Brain tissue
Cerebral edema
Autologous blood
Aquaporin 4
Rat model
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Objective To investigate the neuroprotective effect of [Gly14]-humanin (HNG) in rats with intracerebral hemorrhage (ICH). Methods Thirty healthy male SD rats were randomly divided into 3 groups, namely the sham operated group (10 rats) with needle insertion only, ICH model group (10 rats) with injection of autologous whole blood into the right caudate nucleus, and HNG treatment group (10 rats) with HNG injection into the lateral cerebral ventricle after simulated ICH as in the model group. The changes in the glial cells and cell apoptosis around the hematoma were detected 72 h after the operation. Results The astrocytes and microglial cells in rats receiving HNG injection into the cerebral ventricles showed smaller cell size and shorter and thinner cell processes than those in ICH model group. The numbers of cells positive for glial fibrillary acidic protein (GFAP) and OX42 and the apoptotic cells (as found by TUNEL assay) around the hematoma were significantly reduced in comparison with those in the ICH model group (P<0.05), but still remained significantly higher than those in the sham-operated group (P<0.05). Conclusion HNG can ameliorate the inflammatory response occurring in and around the hematoma and provide some neuroprotection in rats with ICH.
Key words:
[Gly14]-humanin; Intracerebral hemorrhage; Microglia; Apoptosis
Autologous blood
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To explore the protective effects of hirudin on acute experimental intracerebral hemorrhage (ICH) by observing the changes of histologic pathology and brain water content as well as GFAP-positive cells in the perihematomal brain regions.The models of rat ICH were made with infusion of autologous blood into the right neucleus caudatus. The rats were divided randomly into control group, intracerebral hemorrhage group and treating group with hirudin. Brain water content was measured, and pathological and GFAP changes were observed.The pathological impairation after ICH were gradually deteriorated and peaked at the third day. Brain water content after ICH was gradually increased and obviously after one day(P < 0.05) and peaked at the third day. GFAP-positive cells were gradually increased and peaked at the seventh day after ICH. In the treating groups, the pathological impairation and brain water content as well as the GFAP-positive cells were decreased as compared to those in the intracerebral hemorrhage group and the control group. And the positive correlation between GFAP-positive cell numbers and brain water content were shown by linear regression.The local administration of hirudin, a special inhibitor of thrombin, has protective effects within the first week after ICH.
Hirudin
Pulmonary hemorrhage
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Background Endothelin-1 (ET-1) has deleterious effects on water homeostasis, cerebral edema, and blood-brain barrier (BBB) integrity. Highly expressed ET-1 was observed after intracerebral hemorrhage (ICH); however, ET-1 changes and their relationship with BBB disruption within 24 hours of ICH have not been thoroughly investigated. The aim of the present study was to observe the changes in perihematomal ET-1 levels in various phases of ICH and their correlation with the BBB integrity in a rabbit model of ICH. Methods Twenty-five rabbits (3.2–4.3 kg body weight) were randomly divided into a normal control group (five rabbits) and a model group (20 rabbits). Animals in the model group were equally divided into four subgroups (five rabbits each to be sacrificed at 6, 12, 18, and 24 hours following ICH establishment). An ICH model was prepared in the model group by infusing autologous arterial blood into the rabbit brain. ET-1 expression in perihematomal brain tissues was determined using immunohistochemistry and color image analysis, and the permeability of the BBB was assayed using the Evan's Blue (EB) method. A repeated measures analysis of variance was used to make comparisons of the ET-1 and EB content across the entire time series. Results The number of perihematomal endothelial cells with ET-1 positive expressions following 6, 12, 18, and 24 hours ICH model establishment was 9.32, 13.05, 15.90, and 20.44, respectively, but as low as 6.67 in the control group. The average transmittance of ET-1-positive cell bodies at 6, 12, 18, and 24 hours after ICH was 99.10, 97.40, 85.70, and 80.80, respectively, but 100.12 in the control group. These data reveal that the expression of ET-1 was significantly increased at 6, 12, 18, and 24 hours after ICH compared with the control group, and a marked decrease in the average transmittance of ET-1-positive cell bodies was noted ( P <0.05). Similarly, the perihematomal EB content at 6, 12, 18, and 24 hours after ICH was 29.39±1.16, 32.20±0.73, 33.63±1.08, and 35.26±1.12, respectively, in the model group and 28.06±0.80 in the control group. The results indicate that a significant increase in the EB content in the model group was observed compared with that of the control group ( P <0.05). Moreover, a positive correlation between the number of ET-1-positive endothelial cells and BBB permeability was observed ( r =0.883, P <0.05). Conclusions High levels of ET-1 are closely associated with BBB disruption. ET-1 may play an important role in the pathogenesis of secondary brain injury after ICH.
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This study aimed to investigate the effects of thrombin released in hematoma after intracerebral hemorrhage (ICH) on the cerebral injury of perihematomal tissues and to evaluate the protection effect of hirudin on the cerebral injury after ICH.We used the autologous uncoagulated blood injection method to prepare the ICH rat model, and all rats were randomly divided into a normal group, an ICH group, or a hirudin group.At different time points, rat heads were cut to harvest brain sections.Immunohistochemical staining, histochemical staining, and hematoxylin and eosin staining were conducted for CD34, microglia, and neutrocytes.CD34-positive microvessels were most abundant in brain tissues of the sham-operation group.At 12 h after ICH, CD34 expression reduced and reached the minimum level at 72 h (P < 0.01).At 6 h after ICH, microglia expression was visible and reached a peak at 48 h (P < 0.01).At 12 h after ICH, neutrocyte infiltration was visible and the number was greatest at 48 h (P < 0.01).The early application of hirudin after ICH could significantly reduce microglia and neutrocyte expression and could significantly slow down ©FUNPEC-RP www.funpecrp.com.
Hirudin
Microvessel
Infiltration (HVAC)
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Batroxobin
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Abstract This study tested the hypothesis that combined therapy with human umbilical cord‐derived mesenchymal stem cells (HUCDMSCs) and hyperbaric oxygen (HBO) was superior to either one on preserving neurological function and reducing brain haemorrhagic volume (BHV) in rat after acute intracerebral haemorrhage (ICH) induced by intracranial injection of collagenase. Adult male SD rats (n = 30) were equally divided into group 1 (sham‐operated control), group 2 (ICH), group 3 (ICH +HUCDMSCs/1.2 × 10 6 cells/intravenous injection at 3h and days 1 and 2 after ICH), group 4 (ICH +HBO/at 3 hours and days 1 and 2 after ICH) and group 5 (ICH +HUCDMSCs‐HBO), and killed by day 28 after ICH. By day 1, the neurological function was significantly impaired in groups 2‐5 than in group 1 ( P < .001), but it did not differ among groups 2 to 5. By days 7, 14 and 28, the integrity of neurological function was highest in group 1, lowest in group 2 and significantly progressively improved from groups 3 to 5 (all P < .001). By day 28, the BHV was lowest in group 1, highest in group 2 and significantly lower in group 5 than in groups 3/4 (all P < .0001). The protein expressions of inflammation (HMGB1/TLR‐2/TLR‐4/MyD88/TRAF6/p‐NF‐κB/IFN‐γ/IL‐1ß/TNF‐α), oxidative stress/autophagy (NOX‐1/NOX‐2/oxidized protein/ratio of LC3B‐II/LC3B‐I) and apoptosis (cleaved‐capspase3/PARP), and cellular expressions of inflammation (CD14+, F4/80+) in brain tissues exhibited an identical pattern, whereas cellular levels of angiogenesis (CD31+/vWF+/small‐vessel number) and number of neurons (NeuN+) exhibited an opposite pattern of BHV among the groups (all P < .0001). These results indicate that combined HUCDMSC‐HBO therapy offered better outcomes after rat ICH.
Group A
HMGB1
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Background: Intracerebral hemorrhage (ICH) results in secondary brain edema and injury that may lead to death and disability. ICH also causes inflammation. It is unclear whether inflammation contributes to brain edema and neuron injury or functions in repairing the brain tissue. Aims: To understand the effect of inflammation in ICH, we have carried out an investigation on the various aspects and the dynamic changes of inflammation. Settings and Design: An ICH model was generated by injecting 50 ml autologous tail artery blood stereotactically into the right caudate nucleus of 30 rats, which were randomly divided into five ICH groups. Similarly, five Sham control groups were generated by inserting the needle to the right caudate nucleus of rats. Materials and Methods: Rat behavior was evaluated over the time course (6 h, 24 h, 48 h, 72 h and 7 d) in each group. The rats were then killed by administering an overdose of pentobarbital. Following the euthanasia, the brain water content, neuronal loss, glia proliferation, inflammatory infiltration and brain morphology of the rats were measured. Additionally, the expression of TNF-a,IL-6, ICAM-1, VEGF, NF-kB, C3 and CR2 was analyzed by immunohistochemistry. Statistical Analysis: The data were analyzed by student's t test. Results: Rat brain water content increased progressively over the time course and reached its peak at 48h followed ICH. The maximum of inflammatory infiltrate (especially neutrophils) and immunopositive cells of TNF-a, IL-6 and NF-kB, were at 48h. The expression of C3 and CR2 reached their peaks at 48-72h, while the expression ICAM-1 and VEGF were at maximum at 72h followed ICH. Conclusions: The results suggested that the inflammatory cytokines, complement system and VEGF may have a function in the development of the brain edema and neuron injury followed ICH.
Brain Edema
Caudate nucleus
Infiltration (HVAC)
Cerebral edema
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[Dynamic and long-lasting expression of thrombin receptor-1 after intracerebral hemorrhage in rats].
AIM To study the dynamic and long-lasting expression of thrombin receptor after acute intracerebral hemorrhage (ICH) in rats. METHODS 36 rats were randomly divided into 6 groups (n = 6): Normal group and ICH model groups at 6 hours, 24 hours, 3 days, 7 days and 14 days. ICH models were produced with the induction of collagenase type VII-S. Immunohistochemical method was used to detect PAR-1 protein and RT-PCR technique was used to detect PAR-1mRNA in brain tissue around the haematoma in different groups. RESULTS PAR-1 protein and mRNA were mild positive in normal group. In model groups, intensity of PAR-1 expression started to enhance at 6 hours, and enhanced more at 24 hours. PAR-1 expression reached the peak at 3 days and began to descend. At 7 days the descent was obvious and there was further descent at 14 days. At each time point, the PAR-1 protein positive cell number and PAR-1mRNA absorbance ratio in ICH model groups were significantly higher than those in normal group (P < 0.05 or P < 0.01). In addition, PAR-1 proteins were obviously expressed in vivo in brain capillary endothelial cell. CONCLUSION Functional PAR-1 exists in brain capillary endothelial cells. Activation of PAR-1 after ICH due to the stimulation of thrombin is not only the initiating agent of cerebral edema after ICH, but also participates the development of cerebral edema.
Cerebral edema
Brain Edema
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