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Protective effect of hyperin on focal cerebral ischemia reperfusion injury in rats  [cached]
Hong-Yan CHEN,Xin-Bo YANG
Zhong Xi Yi Jie He Xue Bao , 2006,
Abstract: Objective: To investigate the protective effect of hyperin (Hyp) on focal cerebral ischemia reperfusion injury in rats. Methods: Sixty Wistar male rats were randomly divided into sham-operated group, untreated group, and high-, medium- and low-dose Hyp-treated groups(50, 25 and 12.5 mg·kg-1·d-1) and ginkgo leaf-treated group. The animals were intragastrically administered with drugs for 5 days. Thirty minutes after the end administration, the operation was performed to induce the middle cerebral artery occlusion (MCAO) model in rats with the method of intraluminal thread. The middle cerebral artery blood flow was blocked for 2 hours, and then reperfused. Twenty-four hours later, the rats' neurology score was observed. Brain triphenyltetrazolium chloride (TTC) staining and dried wet method were carried out to measure the infarct size and the water content of rat brain tissue respectively. Results: The above-mentioned indexes in the untreated group showed significant differences compared with those in the sham-operated group (P<0.01).The infarct sizes of rat brain tissue in the high- and medium-dose Hyp-treated groups were obviously decreased compared with that in the untreated group (P<0.01, P<0.05). The water content of rat brain and the neurology score were also obviously reduced compared with those in the untreated group (P<0.05 or P<0.01). Conclusions: Hyp could obviously reduce the brain infarct size and cerebral edema degree in focal cerebral ischemia reperfusion injury rats. Hyp has significant protective effect on focal cerebral ischemia reperfusion injury.
Protective Effect of Glycyrrhizin, a Direct HMGB1 Inhibitor, on Focal Cerebral Ischemia/Reperfusion-Induced Inflammation, Oxidative Stress, and Apoptosis in Rats  [PDF]
Gu Gong, Lei Xiang, Libang Yuan, Ling Hu, Wei Wu, Lin Cai, Liang Yin, Hailong Dong
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0089450
Abstract: Aim Glycyrrhizin (GL) has been reported to protect against ischemia and reperfusion (I/R)-induced injury by inhibiting the cytokine activity of high mobility group box 1 (HMGB1). In the present study, the protective effects of GL against I/R injury, as well as the related molecular mechanisms, were investigated in rat brains. Methods Focal cerebral I/R injury was induced by intraluminal filamentous occlusion of the middle cerebral artery (MCA) in Male Sprague-Dawley rats. GL alone or GL and rHMGB1 were administered intravenously at the time of reperfusion. Serum levels of HMGB1 and inflammatory mediators were quantified via enzyme-linked immunosorbent assay (ELISA). Histopathological examination, immunofluorescence, RT-PCR and western blotting analyses were performed to investigate the protective and anti-apoptotic effects and related molecular mechanisms of GL against I/R injury in rat brains. Results Pre-treatment with GL significantly reduced infarct volume and improved the accompanying neurological deficits in locomotor function. The release of HMGB1 from the cerebral cortex into the serum was inhibited by GL administration. Moreover, pre-treatment with GL alleviated apoptotic injury resulting from cerebral I/R through the inhibition of cytochrome C release and caspase 3 activity. The expression levels of inflammation- and oxidative stress-related molecules including TNF-α, iNOS, IL-1β, and IL-6, which were over-expressed in I/R, were decreased by GL. P38 and P-JNK signalling were involved in this process. All of the protective effects of GL could be reversed by rHMGB1 administration. Conclusions GL has a protective effect on ischemia-reperfusion injury in rat brains through the inhibition of inflammation, oxidative stress and apoptotic injury by antagonising the cytokine activity of HMGB1.
Protective effect of low-level laser irradiation on acupuncture points combined with iontophoresis against focal cerebral ischemia-reperfusion injury in rats
DAI Ju-Yun
Zhong Xi Yi Jie He Xue Bao , 2005,
Abstract: Objective: To investigate the effects of low-level laser irradiation on acupuncture points combined with iontophoresis against brain damage after middle cerebral artery occlusion (MCAO) in rats. Methods: Sixty-nine SD rats were randomly divided into five groups, including normal group, sham operation group, model group, electro-acupuncture group and low-level laser irradiation on acupuncture points combined with iontophoresis group (LLLI group). The cerebral ischemia-reperfusion (I/R) model was established by thread embolism of middle cerebral artery. The rats in the LLLI group, as well as the electro-acupuncture group were given treatment as soon as the occlusion finished (0 hour) and 12, 24 hours after the occlusion. We observed the changes of neurological deficit scores and the body weight of the rats at different time. The activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) in the rat’s brain tissue were tested. Results: The neurological deficit score of the LLLI group was significantly lower than that of the model group. The body weight and the activity of SOD of the rats decreased slightly, and the content of MDA decreased significantly after the treatment. Conclusion: The low-level laser irradiation on acupuncture points combined with iontophoresis can prevent focal cerebral ischemia-reperfusion injury. One of its mechanisms may be increasing the activity of SOD and decreasing the damage of the oxidation products to the body.
Reperfusion Promotes Mitochondrial Dysfunction following Focal Cerebral Ischemia in Rats  [PDF]
Jun Li, Xuesong Ma, Wei Yu, Zhangqun Lou, Dunlan Mu, Ying Wang, Baozhong Shen, Sihua Qi
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0046498
Abstract: Background and Purpose Mitochondrial dysfunction has been implicated in the cell death observed after cerebral ischemia, and several mechanisms for this dysfunction have been proposed. Reperfusion after transient cerebral ischemia may cause continued and even more severe damage to the brain. Many lines of evidence have shown that mitochondria suffer severe damage in response to ischemic injury. The purpose of this study was to observe the features of mitochondrial dysfunction in isolated mitochondria during the reperfusion period following focal cerebral ischemia. Methods Male Wistar rats were subjected to focal cerebral ischemia. Mitochondria were isolated using Percoll density gradient centrifugation. The isolated mitochondria were fixed for electron microscopic examination; calcium-induced mitochondrial swelling was quantified using spectrophotometry. Cyclophilin D was detected by Western blotting. Fluorescent probes were used to selectively stain mitochondria to measure their membrane potential and to measure reactive oxidative species production using flow cytometric analysis. Results Signs of damage were observed in the mitochondrial morphology after exposure to reperfusion. The mitochondrial swelling induced by Ca2+ increased gradually with the increasing calcium concentration, and this tendency was exacerbated as the reperfusion time was extended. Cyclophilin D protein expression peaked after 24 hours of reperfusion. The mitochondrial membrane potential was decreased significantly during the reperfusion period, with the greatest decrease observed after 24 hours of reperfusion. The surge in mitochondrial reactive oxidative species occurred after 2 hours of reperfusion and was maintained at a high level during the reperfusion period. Conclusions Reperfusion following focal cerebral ischemia induced significant mitochondrial morphological damage and Ca2+-induced mitochondrial swelling. The mechanism of this swelling may be mediated by the upregulation of the Cyclophilin D protein, the destruction of the mitochondrial membrane potential and the generation of excessive reactive oxidative species.
Reperfusion Promotes Mitochondrial Biogenesis following Focal Cerebral Ischemia in Rats  [PDF]
Yuying Xie, Jun Li, Guibo Fan, Sihua Qi, Bing Li
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0092443
Abstract: Background and Purpose Reperfusion after transient cerebral ischemia causes severe damage to mitochondria; however, little is known regarding the continuous change in mitochondrial biogenesis during reperfusion. Mitochondrial biogenesis causes an increase in the individual mitochondrial mass of neurons and maintains their aerobic set-point in the face of declining function. The aim of this study was to examine mitochondrial biogenesis in the cortex during reperfusion following focal cerebral ischemia. Methods Male Wistar rats were subjected to transient focal cerebral ischemia. The relative amount of cortical mitochondrial DNA was analyzed using quantitative real-time PCR at 0 h, 24 h, 72 h, and 7 d after reperfusion. Three critical transcriptional regulators of mitochondrial biogenesis were measured by semi-quantitative reverse-transcription PCR. The protein expression of cytochrome C oxidase subunits I and IV was detected by Western blotting. Results Evidence of increased mitochondrial biogenesis was observed after reperfusion. The cortical mitochondrial DNA content increased after 24 h, peaked after 72 h, and maintained a high level for 7 d. The cortical expression of three critical genes for the transcriptional regulation of mitochondrial biogenesis, namely, peroxisome proliferator-activated receptor coactivator-1α, nuclear respiratory factor-1, and mitochondrial transcription factor A, also increased at 24 h and 72 h. The expression of peroxisome proliferator-activated receptor coactivator-1α returned to the baseline level at 7 d, but two other factors maintained higher levels compared with the controls. Moreover, the expression of cytochrome C oxidase subunits I and IV was increased in the cortex. Conclusions These results indicate that reperfusion increased mitochondrial biogenesis following focal cerebral ischemia, and this tendency was exacerbated as the reperfusion time was extended. Reperfusion-induced mitochondrial biogenesis was mediated through up-regulation of critical transcriptional regulators of mitochondrial biogenesis.
Neuroprotective Effect of Phosphocreatine on Focal Cerebral Ischemia-Reperfusion Injury
Tiegang Li,Nana Wang,Min Zhao
Journal of Biomedicine and Biotechnology , 2012, DOI: 10.1155/2012/168756
Abstract: Phosphocreatine (PCr) is a natural compound, which can donate high-energy phosphate group to ADP to synthesize ATP, even in the absence of oxygen and glucose. At present, it is widely used in cardiac and renal ischemia-reperfusion (IR) disease. In this study, to examine the protective efficacy of PCr against cerebral IR, disodium creatine phosphate was injected intravenously into rats before focal cerebral IR. Intracranial pressure (ICP), neurological score, cerebral infarction volume, and apoptotic neurons were observed. Expression of caspase-3 and aquaporin-4 (AQP4) was analyzed. Compared with IR group, rats pretreated with PCr had better neurologic score, less infarction volume, fewer ultrastructural histopathologic changes, reduced apoptosis, and lower aquaporin-4 level. In conclusion, PCr is neuroprotective after transient focal cerebral IR injury. Such a protection might be associated with apoptosis regulating proteins.
Functional evaluation of temporary focal cerebral ischemia: experimental model
Duarte, Sinésio Grace;Campos, Ant?nio Dorival;Colli, Benedicto Oscar;
Arquivos de Neuro-Psiquiatria , 2003, DOI: 10.1590/S0004-282X2003000500009
Abstract: objective: despite cerebral ischemia being a frequent clinical pathologic state, the tolerance of neural tissue to oxygen absence and to reperfusion is controversial. this study aims to evaluate the effects of focal cerebral ischemia/reperfusion, by analyzing the mitochondrial respiration. method: sixty-four adult rats underwent focal cerebral ischemia by middle cerebral artery occlusion, during 15, 30 and 60 minutes, followed by 10 minutes or 19 hours of reperfusion. the effects of ischemia were analyzed measuring the o2 consumption by mitochondria in the ischemic and non-ischemic areas. results: there was compromise of the mitochondrial respiration after 30 and 60 minutes of ischemia, followed by 10 minutes of reperfusion but there was no alteration in this function after 19 hours of reperfusion. conclusion: compromise of the mitochondrial function occurred after 30 minutes of ischemia but, until one hour of ischemia, if the reperfusion was prolonged there was no evidence of ischemic/reperfusion injuries.
Functional evaluation of temporary focal cerebral ischemia: experimental model
Duarte Sinésio Grace,Campos Ant?nio Dorival,Colli Benedicto Oscar
Arquivos de Neuro-Psiquiatria , 2003,
Abstract: OBJECTIVE: Despite cerebral ischemia being a frequent clinical pathologic state, the tolerance of neural tissue to oxygen absence and to reperfusion is controversial. This study aims to evaluate the effects of focal cerebral ischemia/reperfusion, by analyzing the mitochondrial respiration. METHOD: Sixty-four adult rats underwent focal cerebral ischemia by middle cerebral artery occlusion, during 15, 30 and 60 minutes, followed by 10 minutes or 19 hours of reperfusion. The effects of ischemia were analyzed measuring the O2 consumption by mitochondria in the ischemic and non-ischemic areas. RESULTS: There was compromise of the mitochondrial respiration after 30 and 60 minutes of ischemia, followed by 10 minutes of reperfusion but there was no alteration in this function after 19 hours of reperfusion. CONCLUSION: Compromise of the mitochondrial function occurred after 30 minutes of ischemia but, until one hour of ischemia, if the reperfusion was prolonged there was no evidence of ischemic/reperfusion injuries.
Biochemical evaluation of focal non-reperfusion cerebral ischemia by middle cerebral artery occlusion in rats
Colli, Benedicto Oscar;Tirapelli, Daniela Pretti da Cunha;Carlotti Jr, Carlos Gilberto;Lopes, Luiza da Silva;Tirapelli, Luis Fernando;
Arquivos de Neuro-Psiquiatria , 2008, DOI: 10.1590/S0004-282X2008000500023
Abstract: cerebral ischemia is an important event in clinical and surgical neurological practice since it is one of the diseases that most compromise the human species. in the present study 40 adult rats were submitted to periods of focal ischemia of 30, 60 and 90 min without reperfusion and animals submitted to a sham procedure were used as controls. we analyzed the levels of atp, malondialdehyde and caspase-3. no significant differences in the biochemical measurements were observed between the right and left brain hemispheres of the same animal in each experimental group. reduced atp levels were observed after the three periods of ischemia compared to the sham group. no significant increase in malondialdehyde or caspase-3 levels was observed. despite significant changes in atp levels, the results indicated cell viability in the ischemic region as shown by the low rates of lipid peroxidation and apoptosis, findings probably related to the lack of reperfusion.
Protective effect of extract of Cordyceps sinensis in middle cerebral artery occlusion-induced focal cerebral ischemia in rats
Zhenquan Liu, Pengtao Li, Dan Zhao, Huiling Tang, Jianyou Guo
Behavioral and Brain Functions , 2010, DOI: 10.1186/1744-9081-6-61
Abstract: The right middle cerebral artery occlusion model was used in the study. The effects of Cordyceps sinensis (Caterpillar fungus) extract on mortality rate, neurobehavior, grip strength, lactate dehydrogenase, glutathione content, Lipid Peroxidation, glutathione peroxidase activity, glutathione reductase activity, catalase activity, Na+K+ATPase activity and glutathione S transferase activity in a rat model were studied respectively.Cordyceps sinensis extract significantly improved the outcome in rats after cerebral ischemia and reperfusion in terms of neurobehavioral function. At the same time, supplementation of Cordyceps sinensis extract significantly boosted the defense mechanism against cerebral ischemia by increasing antioxidants activity related to lesion pathogenesis. Restoration of the antioxidant homeostasis in the brain after reperfusion may have helped the brain recover from ischemic injury.These experimental results suggest that complement Cordyceps sinensis extract is protective after cerebral ischemia in specific way. The administration of Cordyceps sinensis extract significantly reduced focal cerebral ischemic/reperfusion injury. The defense mechanism against cerebral ischemia was by increasing antioxidants activity related to lesion pathogenesis.Ischemic hypoxic brain injury often causes irreversible brain damage. The cascade of events leading to neuronal injury and death in ischemia includes the release of cytokines and free radicals, and induction of inflammation, apoptosis, and excitotoxicity [1]. Reperfusion of ischemic areas could exacerbate ischemic brain damage through the generation of reactive oxygen species. The lack of effective and widely applicable pharmacological treatments for ischemic stroke patients may explain a growing interest in traditional medicines. Recently, from the point of view of "self-medication" or "preventive medicine," several dietary supplements are used in the prevention of life-style related diseases including cerebral
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