[Effect of jianxin pinglu pill on arrhythmia and aquaporin 4 expression in rats with myocardial ischemia/reperfusion injury].
4
Citation
0
Reference
10
Related Paper
Citation Trend
Abstract:
To explore the effect of jianxin pinglu pill (JPP) on arrhythmia and aquaporin 4 (AQP4) in rats with myocardial ischemia/reperfusion (I/R) injury.The effects of JPP on arrhythmia, mortality and AQP4 on I/R injured rats model induced by blocking left coronary artery were observed using II lead of ECG, HE stain and AQP4 immunohistochemical stain.JPP showed significant effect in lowering the arrhythmia occurrence and mortality, reducing myocardial ischemic edema and injury, strengthening AQP4 expression in myocardial tissue.JPP has the effect of preventing I/R induced arrhythmia, it might be related with its action in up-regulating AQP4 expression level in myocardium and reducing the intracellular edema.Keywords:
Aquaporin 4
Stain
Cite
Aquaporin 4
Cerebral edema
Cite
Citations (24)
Objective To investgate the role of aquaporin-4(AQP4) in secondary cerebral edema after ischemia/reperfusion injury in rats.Methods When the models of reversible middle cerebral artery occlusion were established, the alterations of cerebral edema and BBB were evaluated by measuring water and Eval's Blue (EB) contents of cerebral tissue, and the expression of AQP4 in brain was observed by Western Blot at different time point after reperfusion. At last, the correlation between expression of AQP4 and water and EB contents of cerebral tissue were analysed.Results There were found that water and EB contents of cerebral tissue in rat models significantly higher than those of control group at different time point after ischemia/reperfusion ( P0.05~0.01). At the same time, compared with control group, AQP4 expression in cerebral edema group showed obviously statistical increasing(all P0.05). The expression of AQP4 increased gradually after ischemia/reperfusion.It reached the peak between 24 h and 48 h after reperfusion. The positive correlation was found between expression of AQP4 and water and EB contents of cerebral tissue( r=0.38, r=0.45, all P0.05).Conclusions High expression of AQP4 may involve in secondary cerebral edema and BBB opening after cerebral ischemia/reperfusion, and it is an important molecular mechanism of cerebral edema formation.
Aquaporin 4
Cerebral edema
Brain tissue
Cite
Citations (0)
Aquaporin 4
Cite
Citations (26)
AIM: To explore the effects of ghrelin on the brain edema,the permeability of blood-brain barrier(BBB) and the expression of aquaporin 4(AQP4) after cerebral ischemia/reperfusion in rats.METHODS: Adult male Sprague-Dawley rats were randomly divided into sham operation group,middle cerebral artery occlusion(MCAO) group and ghrelin treatment group.The MCAO model was made with nylon thread for 2 h of occlusion following 22 h of reperfusion.Ghrelin at a dose of 10 nmol/kg was injected via femoral vein at the beginning of reperfusion.The cerebral infarct volume was measured by 2,3,5-triphenyltetrazolium chloride(TTC) staining.Brain functional deficits were evaluated by determining the neurological scores.The changes of brain swelling and water content were analyzed through volume calculation and dry/wet weight measurement.The permeability of BBB was detected by collecting extravascular Evans blue(EB) in the brain cortex.The changes of AQP4 expression were assessed by the methods of immunohistochemistry and Western blotting.RESULTS: Compared with MCAO group,the rats in ghrelin treatment group had smaller brain infarct volume,lower EB exudation content and neurological scores.The percentage of brain swelling,water content and AQP4 expression were lower in ghrelin treatment group than those in MCAO group.CONCLUSION: Ghrelin reduces the injury of cerebral ischemia/reperfusion,and lightens the brain edema and BBB damage in rats.Ghrelin also inhibits the expression of AQP4 in brain tissue.
Evans Blue
Aquaporin 4
Cerebral edema
Brain Edema
Brain ischemia
Cite
Citations (0)
Cerebral edema is a major threat for stroke victims. Most studies have focused on the neuroprotective activities of propofol, addressing infarct volume rather than cerebral edema. Aquaporin-4 (AQP4) plays an important role in maintaining brain water homeostasis under various neurological insults. We explored the effect of propofol pretreatment on cerebral edema in a rat model of brain ischemia reperfusion and assessed the involvement of AQP4.To induce brain ischemia reperfusion, we introduced a silicone-coated monofilament nylon suture into the origin of the middle cerebral artery, withdrawing it after 90 min. Treatment groups (n = 32), received propofol (0.1 mL x kg(-1) x min(-1)) infusion for 30 min before occlusion; the vehicle group (n = 32) and the sham-operated group (n = 28), which received the intralipid vehicle at the same time and rate. To assess cerebral infarct volume, we used 2, 3, 5-triphenyl-tetrazolium chloride staining; wet-dry weight ratio was the basis for cerebral edema estimation, and we used immunohistochemistry and Western blot to detect AQP4 expression.The wet-dry weight ratio decreased from 86.89% +/- 0.71% in the vehicle group (n = 6) to 72.42% +/- 0.74% in the propofol group (n = 6), corresponding to an average decrease of 16%. In parallel and based on immunohistochemical semi-quantification, the propofol group exhibited remarkable attenuation of AQP4 over-expression in the ischemic border zone compared with the vehicle group: 1.28 +/- 0.03 vs 1.40 +/- 0.05, n = 7, respectively; P < 0.05. Values derived from Western blot quantification were similarly decreased in the propofol group compared to the vehicle group: 20.85% +/- 4.18% vs 31.67% +/- 3.23%, n = 4, respectively; P < 0.05. However, infarct volume and neurologic deficit in postischemic rats in the propofol group were not statistically different from values in the vehicle group.We conclude that prestroke treatment with propofol reduces postischemic cerebral edema in rats, possibly through inhibiting AQP4 over-expression in the boundary zone of ischemia.
Aquaporin 4
Cerebral edema
Cite
Citations (52)
Objective:By immunohistochemistry and compute-assisted image analysis,We investigated the changes in protein expression of ACTH levels in rat brain during reperfusion after ischemia. Methods: 70 male wistar rats randomly divided into 3 groups: normal control group (n=10),sham-ischemia group(n=30), cerebral ischemia-reperfusion group(n=30). Temporary cerebral ischemia-reperfusion injury model was established by using common carotid artery blood drainage Methods: Brain section was obtained by cryostat sectioning. The section was prepared for ACTH immunohistochemistry staining and was observed by optical microscope. Quantitate analysis was carried out for ACTH immunoreactive matter stain area and density. Results: During ischemia reperfusion, The expression of ACTH protein in brain is increased sharply at 6h and 24h, and fallback to the control level at 72h. Conclusions:The present results demonstrate that the sharply expression of ACTH protein in brain at early reperfusion might be one of the mechanism for delayed brain ischemia reperfusion injury.
Stain
Brain ischemia
Cite
Citations (0)
Objective To investigate the source and effects of tumour necrosis factor (TNF α) in the model of rat pups after gut ischemia/reperfusion (I/R) injury.Methods 1. Forty eight male Wistar rat pups (wt.130±15?g) were randomly divided into six groups (8 for each group): 1) sham operation group (SG), 2) ischemia 30'group (I30'G), 3) ischemia 30'/reperfusion30'group (I30'/R30'G), 4) ischemia30'/ reperfusion 60'group (I30'/R60'G), 5) ischemia30'/reperfusion90' group ( I30'/R90'G), 6) ischemia 120' group (I120'G). 2.Using SP immunohistochemistry, the expression and distribution of TNF α in the gut and liver were assessed. 3. The pathologic changes of gut were observed by H. E staining. Results 1.TNF α positive material stained strongly in gut mucosal cells in I30'G ,I30'/R60'G ,I30'/R90'G; very strongly in I30'/R30'G and 120'G.2.TNF α appeared weak in I30'G in liver; moderately in I30'/R30'G and I30'/R60'G;stongly in I30'/90'G and I120'G.3. The gut mucosal villi were weakly damaged with edema in I30'G; more seriously with necrosis or hemorrhage in I30'/R30'G and I120'G.Conclusions TNF α appears in the cytoplasm of gut and liver in the rat pup model after gut I/R injury. Compared with in the liver tissue, TNF α stains more strongly in the gut. This suggests the gut might be the major source of TNF α, which mediates gut I/R injury.
Cite
Citations (0)
To investigate the effects of transient cerebral ischemia and reperfusion injury on brain edema and apoptosis hippocampal neurons of aged animals.120 19-21-month-old healthy Wistar rats underwent four-vessel occlusion to establish whole cerebral ischemia model and were randomly divided into 3 equal groups to undergo ischemia for 1 min, 3 min, and 5 min respectively. Every group was re-divided into 5 equal sub-groups to undergo reperfusion for 12 h, 1 d, 2 d, 3 d, and 7 d respectively. Another 40 rats underwent sham operation to be used as controls. At different reperfusion time points 4 rats from each subgroup were killed to measure the wet and dry weights of the hippocampus. The brains of the remaining 4 rats from each subgroup underwent HE staining and microscopy. The expression of aquaporin-4 (AQP4) was detected by SABC immunohistochemical technique, and the neuron apoptosis in hippocampus was detected by TUNEL method.There was no significant differences in brain water content and expression of AQP4 between the ischemia 1 min and 3 min subgroups and the corresponding sham-operation subgroups (all P > 0.05), however, the brain water contents and AQP4 expression levels of the ischemia 5 min subgroups were all significantly higher than those of the corresponding sham-operation subgroups (all P < 0.05). There were only a few TUNEL-positive cells in the sham-operation subgroups and ischemia 1 min subgroups, however, the numbers of TUNEL-positive cells of the ischemia 3 min and 5 min subgroups were all significantly higher. The number of TUNEL-positive cells raised 12 h after ischemia, peaked 1 day after, and began to go down 3 days later.The aged animals are more sensitive to cerebral ischemia/reperfusion injury, and transient cerebral ischemia may cause brain edema, and increase of apoptotic cells and AQP4 expression. Neuron apoptosis is more sensitive to cerebral ischemia than brain edema and AQP4 expression. After reperfusion neuron apoptosis peaks earlier and lasts longer in the aged animals.
Aquaporin 4
Brain ischemia
Cite
Citations (3)