共查询到20条相似文献,搜索用时 31 毫秒
1.
Tu XK Yang WZ Liang RS Shi SS Chen JP Chen CM Wang CH Xie HS Chen Y Ouyang LQ 《Neurochemical research》2011,36(11):2022-2028
Focal cerebral ischemia results in an increased expression of matrix metalloproteinase-9 (MMP-9), which induces vasogenic
brain edema via disrupting the blood–brain barrier (BBB) integrity. Recent studies from our laboratory showed that baicalin
reduces ischemic brain damage by inhibiting inflammatory reaction and neuronal apoptosis in a rat model of focal cerebral
ischemia. In the present study, we first explored the effect of baicalin on the neuronal damage, brain edema and BBB permeability,
then further investigated its potential mechanisms. Sprague–Dawley rats underwent permanent middle cerebral artery occlusion
(MCAO). Baicalin was administrated by intraperitoneally injected twice at 2 and 12 h after the onset of MCAO. Neuronal damage,
brain edema and BBB permeability were measured 24 h following MCAO. Expression of MMP-9 protein and mRNA were determined by
western blot and RT–PCR, respectively. Expression of tight junction protein (TJP) occludin was detected by western blot. Neuronal
damage, brain edema and BBB permeability were significantly reduced by baicalin administration following focal cerebral ischemia.
Elevated expression of MMP-9 protein and mRNA were significantly down-regulated by baicalin administration. In addition, MCAO
caused the decreased expression of occludin, which was significantly up-regulated by baicalin administration. Our study suggested
that baicalin reduces MCAO-induced neuronal damage, brain edema and BBB permeability, which might be associated with the inhibition
of MMP-9 expression and MMP-9-mediated occludin degradation. 相似文献
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Bernhard Metzler Johannes Jehle Igor Theurl Susanne Ludwiczek Peter Obrist Otmar Pachinger Günter Weiss 《Biometals》2007,20(2):205-215
The role of iron in the pathogenesis of cardio-vascular disorders is still controversial. We studied the effects of iron perturbations
on myocardial injury upon temporary ischemia/reperfusion. C57BL/6J male mice were injected with iron dextran for 2 weeks while
controls received saline. Mice were then subjected to 30 min of myocardial ischemia and subsequent reperfusion for 6–24 h.
Tissue damage was quantified histologically and by troponin T determination. The expressions of tumor necrosis factor-α (TNF-α),
superoxide dismutase (SOD) and inducible nitric oxide synthase (iNOS) were investigated in non-ischemic and ischemic regions
of both groups. After myocardial ischemia and reperfusion, troponin T levels, as a marker of myocardial damage, were significantly
reduced in iron-treated mice as compared to control mice (P < 0.05). Under the same conditions the infarction area and damage score were significantly lower in iron-treated animals.
In parallel, TNF-α and SOD expressions were increased in infarcted regions of iron-treated mice as compared to controls, whereas
myocardial iNOS expression was significantly lower in iron-treated mice. Although, iron challenge increased radical formation
and TNF-α expression in vivo, this did not result in myocardial damage which may be linked to the parallel induction of SOD. Importantly, iron treatment
inhibited iNOS expression. Since, an increased nitric oxide (NO) formation has been linked to cardiac damage after acute myocardial
infarction, iron may exert short time cardio-protective effects after induction of ischemia/reperfusion via decreasing iNOS
formation.
Both authors contributed equally to this work. 相似文献
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Li Q Huang XJ He W Ding J Jia JT Fu G Wang HX Guo LJ 《Cellular and molecular neurobiology》2009,29(2):169-180
We previously reported that inhibition of Rho-kinase (ROCK) by hydroxyl fasudil improves cognitive deficit and neuronal damage
in rats with chronic cerebral ischemia (Huang et al., Cell Mol Neurobiol 28:757–768, 2008). In this study, fasudil mesylate
(FM) was investigated for its neuroprotective potential in rats with ischemia following middle cerebral artery occlusion (MCAO)
and reperfusion. The effect of fasudil mesylate was also studied in rat brain cortical and hippocampal slices treated with
oxygen-glucose deprivation (OGD) injury. Gross anatomy showed that cerebral infarct size, measured with 2,3,5-triphenyltetrazolium
chloride (TTC) staining, was significantly smaller in the FM-treated than in the non-FM-treated ischemic rats. In the brain
regions vulnerable to ischemia of ischemic rats, fasudil mesylate was also found to significantly restore the enzyme protein
expression level of endothelial nitric oxide synthase (eNOS), which was decreased in ischemia. However, it remarkably reduced
the protein synthesis of inducible nitric oxide synthase (iNOS) that was induced by ischemia and reperfusion. In rat brain
slices treated with OGD injury, fasudil mesylate increased the neuronal cell viability by 40% for cortex and by 61% for hippocampus,
respectively. Finally, in the presence of OGD and fasudil mesylate, superoxide dismutase (SOD) activity was increased by 50%
for cortex and by 58% for hippocampus, compared to OGD only group. In conclusion, our in vivo study showed that fasudil mesylate
not only decreased neurological deficit but also reduced cerebral infarct size, possibly and at least partially by augmenting
eNOS protein expression and inhibiting iNOS protein expression after ischemia-reperfusion.
Xian-Ju Huang contributed equally to this article. 相似文献
7.
Bing Zhao Meng Zhang Xue Han Xia-Yan Zhang Qiong Xing Xu Dong Qiao-Juan Shi Peng Huang Yun-Bi Lu Er-Qing Wei Qiang Xia Wei-Ping Zhang Chun Tang 《PloS one》2013,8(12)
Intracellular nicotinamide phosphoribosyltransferase (iNAMPT) in neuron has been known as a protective factor against cerebral ischemia through its enzymatic activity, but the role of central extracellular NAMPT (eNAMPT) is not clear. Here we show that eNAMPT protein level was elevated in the ischemic rat brain after middle-cerebral-artery occlusion (MCAO) and reperfusion, which can be traced to at least in part from blood circulation. Administration of recombinant NAMPT protein exacerbated MCAO-induced neuronal injury in rat brain, while exacerbated oxygen-glucose-deprivation (OGD) induced neuronal injury only in neuron-glial mixed culture, but not in neuron culture. In the mixed culture, NAMPT protein promoted TNF-α release in a time- and concentration-dependent fashion, while TNF-α neutralizing antibody protected OGD-induced, NAMPT-enhanced neuronal injury. Importantly, H247A mutant of NAMPT with essentially no enzymatic activity exerted similar effects on ischemic neuronal injury and TNF-α release as the wild type protein. Thus, eNAMPT is an injurious and inflammatory factor in cerebral ischemia and aggravates ischemic neuronal injury by triggering TNF-α release from glia cells, via a mechanism not related to NAMPT enzymatic activity. 相似文献
8.
Gaire Bhakta Prasad Kwon Oh Wook Park Sung Hyuk Chun Kwang-Hoon Kim Sun Yeou Shin Dong Yun Choi Ji Woong 《PloS one》2015,10(3)
Paradols are non-pungent and biotransformed metabolites of shogaols and reduce inflammatory responses as well as oxidative stress as shogaols. Recently, shogaol has been noted to possess therapeutic potential against several central nervous system (CNS) disorders, including cerebral ischemia, by reducing neuroinflammation in microglia. Therefore, paradol could be used to improve neuroinflammation-associated CNS disorders. Here, we synthesized paradol derivatives (2- to 10-paradols). Through the initial screening for anti-inflammatory activities using lipopolysaccharide (LPS)-stimulated BV2 microglia, 6-paradol was chosen to be the most effective compound without cytotoxicity. Pretreatment with 6-paradol reduced neuroinflammatory responses in LPS-stimulated BV2 microglia by a concentration-dependent manner, which includes reduced NO production by inhibiting iNOS upregulation and lowered secretion of proinflammatory cytokines (IL-6 and TNF-α). To pursue whether the beneficial in vitro effects of 6-paradol leads towards in vivo therapeutic effects on transient focal cerebral ischemia characterized by neuroinflammation, we employed middle cerebral artery occlusion (MCAO)/reperfusion (M/R). Administration of 6-paradol immediately after reperfusion significantly reduced brain damage in M/R-challenged mice as assessed by brain infarction, neurological deficit, and neural cell survival and death. Furthermore, as observed in cultured microglia, 6-paradol administration markedly reduced neuroinflammation in M/R-challenged brains by attenuating microglial activation and reducing the number of cells expressing iNOS and TNF-α, both of which are known to be produced in microglia following M/R challenge. Collectively, this study provides evidences that 6-paradol effectively protects brain after cerebral ischemia, likely by attenuating neuroinflammation in microglia, suggesting it as a potential therapeutic agent to treat cerebral ischemia. 相似文献
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Hiroto Uchida Yuki Fujita Misato Matsueda Masahiro Umeda Shunsuke Matsuda Hiroyuki Kato Jiro Kasahara Tsutomu Araki 《Cellular and molecular neurobiology》2010,30(7):1125-1134
Focal brain lesions such as transient focal cerebral ischemia can lead to neuronal damage in remote areas, including the ipsilateral
substantia nigra and hippocampus, as well as in the ischemic core. In this study, we investigated acute changes in the ipsilateral
hippocampus from 1 up to 7 days after 90 min of transient focal cerebral ischemia in rats, using anti-NeuN (neuronal nuclei),
anti-Cu/Zn-superoxide dismutase (Cu/Zn-SOD), anti-Mn-SOD, anti-neuronal nitric oxide synthase (nNOS), anti-inducible NOS (iNOS),
anti-glial fibrillary acidic protein (GFAP), anti-ionized calcium-binding adaptor molecule 1(Iba 1) and anti-2′,3′-cyclic
nucleotide 3′-phosphodiesterase (CNPase) antibodies. In our western blot and histochemical analyses, present results show
that transient focal cerebral ischemia in rats can cause a severe and acute damage of neurons and oligodendrocytes in the
ipsilateral hippocampal CA1 sector. The present findings also demonstrate that the expression of iNOS produced by Iba 1-immunopositive
microglia precedes the damage of neurons and oligodendrocytes in the ipsilateral hippocampal CA1 sector after transient focal
cerebral ischemia. In contrast, our results suggest that increased reactive oxygen species (ROS) production during reperfusion
cannot lead to damage of neurons and oligodendrocytes in the ipsilateral hippocampal CA1 sector after transient focal cerebral
ischemia, because of an insufficient expression of Cu/Zn-SOD and Mn-SOD. Our double-labeled immunohistochemical study demonstrates
that the overexpression of iNOS produced by Iba 1-immunopositive microglia may play a pivotal role in the damage of neurons
and oligodendrocytes in the ipsilateral hippocampal CA1 sector at an acute stage after transient focal cerebral ischemia. 相似文献
11.
Cai F Li CR Wu JL Chen JG Liu C Min Q Yu W Ouyang CH Chen JH 《Mediators of inflammation》2006,2006(5):30490
Theaflavin, a major constituent of black tea, possesses biological functions such as the antioxidative, antiviral, and anti-inflammatory ones. The purpose of this study was to verify whether theaflavin reduces focal cerebral ischemia injury in a rat model of middle cerebral artery occlusion (MCAO). Male Sprague-Dawley rats were anesthetized and subjected to 2 hours of MCAO followed 24 hours reperfusion. Theaflavin administration (5, 10, and 20 mg/kg, i.v.) ameliorated infarct and edema volume. Theaflavin inhibited leukocyte infiltration and expression of ICAM-1, COX-2, and iNOS in injured brain. Phosphorylation of STAT-1, a protein which mediates intracellular signaling to the nucleus, was enhanced 2-fold over that of sham group and was inhibited by theaflavin. Our study demonstrated that theaflavin significantly protected neurons from cerebral ischemia-reperfusion injury by limiting leukocyte infiltration and expression of ICAM-1, and suppressing upregulation of inflammatory-related prooxidative enzymes (iNOS and COX-2) in ischemic brain via, at least in part, reducing the phosphorylation of STAT-1. 相似文献
12.
Hong-Xia Niu Jun-Zhe Wang Dong-Liang Wang Jun-Jie Miao Hua Li Zhi-Gang Liu Xing Yuan Wei Liu Jing-Ru Zhou 《Cellular and molecular neurobiology》2018,38(2):459-466
Inhibition of ionotropic glutamate receptors (iGluRs) is a potential target of therapy for ischemic stroke. Perampanel is a potent noncompetitive α-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptor (AMPAR) antagonist with good oral bioavailability and favorable pharmacokinetic properties. Here, we investigated the potential protective effects of perampanel against focal cerebral ischemia in a middle cerebral artery occlusion (MCAO) model in rats. Oral administration with perampanel significantly reduced MCAO-induced brain edema, brain infarct volume, and neuronal apoptosis. These protective effects were associated with improved functional outcomes, as measured by foot-fault test, adhesive removal test, and modified neurological severity score (mNSS) test. Importantly, perampanel was effective even when the administration was delayed to 1 h after reperfusion. The results of enzyme-linked immunosorbent assay (ELISA) showed that perampanel significantly decreased the expression of pro-inflammatory cytokines IL-1β and TNF-α, whereas it increased the levels of anti-inflammatory cytokines IL-10 and TGF-β1 after MCAO. In addition, perampanel treatment markedly decreased the expression of inducible nitric oxide synthase (iNOS) and neuronal nitric oxide synthase (nNOS), and also inhibited nitric oxide (NO) generation in MCAO-injured rats at 24 and 72 h after reperfusion. In conclusion, this study demonstrated that the orally active AMPAR antagonist perampanel protects against experimental ischemic stroke via regulating inflammatory cytokines and NOS pathways. 相似文献
13.
Neuroendocrine mechanism for tolerance to cerebral ischemia-reperfusion injury in male rats 总被引:2,自引:0,他引:2
Yang SH Liu R Wen Y Perez E Cutright J Brun-Zinkernagel AM Singh M Day AL Simpkins JW 《Journal of neurobiology》2005,62(3):341-351
Testosterone has been shown to exacerbate cerebral ischemia-reperfusion injury, which suggests that the well-known stress-induced testosterone reduction could be a protective response. We hypothesized that stress-induced testosterone reduction contributes to ischemia tolerance in cerebral ischemia-reperfusion injury in male rats. In intact male rats, stress was induced by brief anesthesia at 6 h before transient middle cerebral artery occlusion (MCAO). Testosterone levels were significantly decreased 6 h after stress. Testosterone reduction was associated with a 50% reduction in cerebral lesion volume in the stressed animals. Further, the stress-induced cerebral ischemia tolerance was eliminated by testosterone replacement in castrated males. Immunohistochemical staining showed that androgen receptors were up-regulated after cerebral ischemia-reperfusion injury and partially colocalized with terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) positive cells in the parietal cortex and extensively colocalized in the caudate putamen. Heat shock protein 70 (Hsp70) and 90 (Hsp90) are involved in ischemia tolerance, and were not colocalized with TUNEL in the immunohistochemical staining, suggesting an antiapoptotic role of Hsp's. To determine the effect of testosterone on MCAO-induced Hsp70 and -90 expression, a testosterone replacement or withdrawal paradigm was used. Testosterone-replaced animals exhibited a decrease in Hsp expression, whereas testosterone withdrawal (mimicking the stress-induced testosterone suppression) normalized this deficit. In summary, stress-induced testosterone reduction contributes to ischemia tolerance in cerebral ischemia-reperfusion injury in males, which could be related to the loss of inhibition by testosterone of Hsp70 and -90 expression. 相似文献
14.
Nakaizumi A Horie T Kida T Kurimoto T Sugiyama T Ikeda T Oku H 《Cellular and molecular neurobiology》2012,32(1):95-106
Modulation of enzyme activity through nitrosylation has recently been identified as a new physiological activity of nitric
oxide (NO). We hypothesized that NO enhances the TNF-α-induced death of retinal neurons through a suppression of nuclear factor-κB
(NF-κB) by nitrosylation. In this study, cells from the RGC-5 line were exposed to different concentrations (2.0, 10, and
50 ng/ml) of TNF-α, and the degree of TNF-α-induced cell death was determined by the WST-8 assay and by flow cytometric measurements
of the externalization of phosphatidylserine. The effects of etanercept, a soluble TNFR-Fc fusion protein, and S-nitroso-N-penicillamine (SNAP), an NO donor, on the toxicity were determined. Experiments were also performed to determine whether
nitric oxide synthase (NOS) was associated with the toxicity of TNF-α. The activation of NF-κB was determined by the detection
of the p65 subunit in the nuclear extracts. Our results showed that exposure of RGC-5 cells to different concentrations of
TNF-α significantly decreased the number of living cells in a dose-dependent way. The death was partially due to apoptosis
with an externalization of phosphatidylserine, and the death was suppressed by etanercept. Exposure to TNF-α increased the
activation of NF-κB and the expression of iNOS. Although NF-κB inhibitors suppressed the increase of iNOS, they also potentiated
the TNF-α-induced death. Both L-NAME and aminoguanidine, both NOS inhibitors, rescued the cells from death. In contrast, addition
of SNAP caused nitrosylation of the inhibitory κB kinase, and suppressed the NF-κB activation and potentiated the TNF-α-induced
neurotoxicity. These results indicate that NO potentiates the neurotoxicity of TNF-α by suppressing NF-κB. 相似文献
15.
甘珀酸干预对大鼠脑缺血再灌注损伤的影响 总被引:1,自引:0,他引:1
目的观察缝隙连接阻断剂甘珀酸对局灶性脑缺血/再灌注损伤的影响。方法采用大鼠大脑中动脉阻塞再灌流模型(MCAO),将动物随机分为脑缺血60min再灌注(MCAO)组,脑缺血再灌注加甘珀酸干预(MCAO+CBX)组和假手术组(sham)。采用尼氏染色显示脑梗死灶并计算梗死灶体积;应用免疫荧光与TUNEL染色法分别观察脑缺血后3d与7d不同时间点缺血边缘区胶质纤维酸性蛋白(GFAP)的表达和细胞凋亡情况。结果(1)缺血后3d、7d MCAO+CBX组大鼠梗死体积小于MCAO组,3d、7d MCAO+CBX组大鼠梗死体积较MCAO组分别缩小5%和4.6%;(2)缺血后3d、7d于缺血边缘区可见大量TUNEL阳性染色细胞,且MCAO组大鼠缺血边缘区细胞凋亡数目明显多于MCAO+CBX大鼠(P〈0.001);(3)缺血后3d和7d组缺血边缘区GFAP表达明显增强,3d的MCAO组与MCAO+CBX组大鼠缺血边缘区GFAP的表达均较假手术组强(P〈0.05),7d的MCAO+CBX组大鼠缺血边缘区GFAP的表达较假手术组强(P〈0.001),但明显弱于MCAO组大鼠(P〈0.01);结论缝隙连接阻断剂甘珀酸可减少大鼠大脑中动脉阻塞后脑梗死体积,其机制可能与阻断缝隙连接后缺血边缘区神经元凋亡降低有关,星型胶质细胞的反应性变化参与了该过程。 相似文献
16.
Aims Taurine as an endogenous substance possesses a number of cytoprotective properties. In the study, we have evaluated the neuroprotective
effect of taurine and investigated whether taurine exerted neuroprotection through affecting calpain/calpastatin or caspase-3
actions during focal cerebral ischemia, since calpain and caspase-3 play central roles in ischemic neuronal death. Methods Male Sprague–Dawley rats were subjected to 2 h of middle cerebral artery occlusion (MCAo), and 22 h of reperfusion. Taurine
was administrated intravenously 1 h after MCAo. The dose–responses of taurine to MCAo were determined. Next, the effects of
taurine on the activities of calpain, calpastatin and caspase-3, the levels of calpastatin, microtubule-associated protein-2
(MAP-2) and αII-spectrin, and the apoptotic cell death in penumbra were evaluated. Results Taurine reduced neurological deficits and decreased the infarct volume 24 h after MCAo in a dose-dependent manner. Treatment
with 50 mg/kg of taurine significantly increased the calpastatin protein levels and activities, and markedly reduced the m-calpain
and caspase-3 activities in penumbra 24 h after MCAo, however, it had no significant effect on μ-calpain activity. Moreover,
taurine significantly increased the MAP-2 and αII-spectrin protein levels, and markedly reduced the ischemia-induced TUNEL
staining positive score within penumbra 24 h after MCAo. Conclusions Our data demonstrate the dose-dependent neuroprotection of taurine against transient focal cerebral ischemia, and suggest
that one of protective mechanisms of taurine against ischemia may be blocking the m-calpain and caspase-3-mediated apoptotic
cell death pathways. 相似文献
17.
Tumor necrosis factor-α (TNF-α) is released from blood-free perfused rat liver by the fungal metabolite ochratoxin A. Here
we have identified Kupffer cells as the sole source of OTA-mediated cytokine release. If single cell preparation of Kupffer
cells, hepatocytes, or sinusoidal endothelial cells were prepared from rat livers, only Kupffer cells released TNF-α upon
incubation with 2.5 μmol/l OTA. OTA failed to induce TNF-α release in the blood-free perfused isolated rat liver when Kupffer
cells were blockedin vitro by 15 μmol/l gadolinium chloride. When rats were pretreatedin vivo with the Kupffer cell depleting clodronate liposomes, OTA-mediated TNF-α release was abrogated in the isolated perfused liver
model. 相似文献
18.
目的:探讨梓醇对缺血再灌注大鼠脑损伤后的保护作用.方法:采用传统大脑中动脉阻塞(MCAO)方法制备大鼠局灶性缺血模型,根据随机数字表法将SD大鼠分为MCAO组、对照组(vehicle组)及梓醇处理组(catalpol组),缺血再灌注48 h后观察各组大鼠神经功能学评分和脑梗死容积.分别于术前、术后6h、24 h、48 h取大鼠脑组织样本,检测匀浆中谷胱甘肽过氧化物酶(GSH-PX)和丙二醛(MDA)的变化情况.结果:与vehicle组和MCAO组相比,catalpol处理组神经功能学评分降低(P<0.05);其梗死容积较小(P<0.05).组织匀浆结果显示catalpol处理组脑匀浆中GSH-PX活力升高,MDA含量下降(P<0.05).结论:梓醇可能通过降低脑内自由基水平、控制脂质过氧化程度,对缺血再灌注引起的大鼠脑损伤产生神经保护作用. 相似文献
19.
The capacity of cornel iridoid glycoside (CIG) to suppress the manifestations of ischemic stroke was investigated. CIG was
administered to rats by the intragastric route once daily for 7 days. Focal cerebral ischemia was induced by 2 h of middle
cerebral artery occlusion followed by 24 h of reperfusion. In non-treated rats large infarct areas were observed within 24 h
of reperfusion. Examination of the ischemic cerebral cortex revealed microglia and astrocyte activation, increased interleukin-1β
(IL-1 β) and tumor necrosis factor-α (TNF-α) concentrations, increased DNA fragmentation in the ischemia penumbra, elevated
Bax expression, increased caspase-3 cleavage, and decreased Bcl-2 expression. Pretreatment with CIG decreased the infarct
area, DNA fragmentation, IL-1β and TNF-α concentrations, microglia and astrocyte activation, Bax expression, and caspase-3
cleavage while increasing Bcl-2 expression. CIG exerts anti-neuroinflammatory and anti-apoptotic effects which should prove
beneficial for prevention or treatment of stroke. 相似文献
20.
Aims Some data have shown the functional connection between calpain and caspase-3. Here, we investigated the cross-talk between
calpain and caspase-3 in penumbra and core during focal cerebral ischemia-reperfusion.
Methods The activities of calpain and the levels of calpastatin, microtubule-associated protein-2 (MAP-2), and spectrin in penumbra
and core at 3 or 23 h of reperfusion (R 3 h or R 23 h) after 1-h focal cerebral ischemia in rats were determined in sham-
or caspase-3 inhibitor z-DEVD-CHO-treated rats.On the other hand, the determination of the activities of caspase-3 and the
levels of MAP-2 and spectrin was done in sham- or calpain-inhibitor I-treated rats.
Results z-DEVD-CHO (600 ng/rat, i.c.v.) markedly reduced the μ- and m-calpain activities in penumbra and the m-calpain activities
in core at R 3 h and R 23 h, and enhanced the calpastatin levels in penumbra at R 3 h and in core at R 3 h and R 23 h significantly;
however, it had no significant effects on the μ-calpain activities in core and the calpastatin levels in penumbra at R 23 h.
Calpain inhibitor I (0.8 mg/rat, i.c.v.) markedly reduced the caspase-3 activities in core at R 3 h and R 23 h, but not in
penumbra. Both calpain and caspase-3 inhibitors increased the levels of MAP-2 and spectrin in penumbra and core significantly
after focal cerebral ischemia-reperfusion.
Conclusions Our data provide direct evidence to demonstrate the cross-talk between calpain and caspase-3 in penumbra and core during focal
cerebral ischemia-reperfusion. 相似文献