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1.
Joon Ha Park Ok kyu Park Jeong-Hwi Cho Bai Hui Chen In Hye Kim Ji Hyeon Ahn Jae-Chul Lee Bing Chun Yan Ki-Yeon Yoo Choong Hyun Lee In Koo Hwang Seung-Hae Kwon Yun Lyul Lee Moo-Ho Won Jung Hoon Choi 《Neurochemical research》2014,39(7):1300-1312
Tanshinone I (TsI) is an important lipophilic diterpene extracted from Danshen (Radix Salvia miltiorrhizae) and has been used in Asia for the treatment of cerebrovascular diseases such as ischemic stroke. In this study, we examined the neuroprotective effect of TsI against ischemic damage and its neuroprotective mechanism in the gerbil hippocampal CA1 region (CA1) induced by 5 min of transient global cerebral ischemia. Pre-treatment with TsI protected pyramidal neurons from ischemic damage in the stratum pyramidale (SP) of the CA1 after ischemia–reperfusion. The pre-treatment with TsI increased the immunoreactivities and protein levels of anti-inflammatory cytokines [interleukin (IL)-4 and IL-13] in the TsI-treated-sham-operated-groups compared with those in the vehicle-treated-sham-operated-groups; however, the treatment did not increase the immunoreactivities and protein levels of pro-inflammatory cytokines (IL-2 and tumor necrosis factor-α). On the other hand, in the TsI-treated-ischemia-operated-groups, the immunoreactivities and protein levels of all the cytokines were maintained in the SP of the CA1 after transient cerebral ischemia. In addition, we examined that IL-4 injection into the lateral ventricle did not protect pyramidal neurons from ischemic damage. In conclusion, these findings indicate that the pre-treatment with TsI can protect against ischemia-induced neuronal death in the CA1 via the increase or maintenance of endogenous inflammatory cytokines, and exogenous IL-4 does not protect against ischemic damage. 相似文献
2.
Joon Ha Park Bich Na Shin Ji Hyeon Ahn Jeong-Hwi Cho In Hye Kim Dae Won Kim Moo-Ho Won Seongkweon Hong Jun Hwi Cho Choong-Hyun Lee 《Cellular and molecular neurobiology》2016,36(5):821-828
Proline-rich Akt substrate of 40-kDa (PRAS40) is one of the important interactive linkers between Akt and mTOR signaling pathways. The increase of PRAS40 is related with the reduction of brain damage induced by cerebral ischemia. In the present study, we investigated time-dependent changes in PRAS40 and phospho-PRAS40 (p-PRAS40) immunoreactivities in the hippocampal CA1 region of the gerbil after 5 min of transient cerebral ischemia. PRAS40 immunoreactivity in the CA1 region was decreased in pyramidal neurons from 12 h after ischemic insult in a time-dependent manner, and, at 5 days post-ischemia, PRAS40 immunoreactivity was newly expressed in astrocytes. p-PRAS40 immunoreactivity in the CA1 pyramidal neurons was hardly found 12 h and apparently detected again 1 and 2 days after ischemic insult. At 5 days post-ischemia, p-PRAS40 immunoreactivity in the CA1 pyramidal neurons was not found. These results indicate that ischemia-induced changes in PRAS40 and p-PRAS40 immunoreactivities in CA1 pyramidal neurons and astrocytes may be closely associated with delayed neuronal death in the hippocampal CA1 region following transient cerebral ischemia. 相似文献
3.
Joon Ha Park YooHun Noh Sung-Su Kim Ji Hyeon Ahn Taek Geun Ohk Jun Hwi Cho Tae-Kyeong Lee Hyunjung Kim Minah Song Jae-Chul Lee Moo-Ho Won Choong-Hyun Lee 《Neurochemical research》2018,43(11):2102-2110
Macrophage inflammatory protein-3α (MIP-3α) and its sole receptor, CCR6, play pivotal roles in neuroinflammatory processes induced by brain ischemic insults. In this study, we investigated transient ischemia-induced changes in MIP-3α and CCR6 protein expressions in the hippocampal CA1 area following 5 min of transient global cerebral ischemia (tgCI) in gerbils. Both MIP-3α and CCR6 immunoreactivities were very strongly expressed in pyramidal neurons of the CA1 area from 6 h to 1 day after tgCI and were hardly shown 4 days after tgCI. In addition, strong MIP-3α immunoreactivity was newly expressed in astrocytes 6 h after tgCI. These results indicate that tgCI causes apparent changes in MIP-3α and CCR6 expressions in pyramidal neurons and astrocytes in the hippocampal CA1 area and suggest that tgCI-induced changes in MIP-3α and CCR6 expressions might be closely associated with neuroinflammatory processes in brain ischemic regions. 相似文献
4.
Park JH Joo HS Yoo KY Shin BN Kim IH Lee CH Choi JH Byun K Lee B Lim SS Kim MJ Won MH 《Neurochemical research》2011,36(11):2043-2050
The fruit of Terminalia chebula Retz has been used as a traditional medicine in Asia and contains tannic acid, chebulagic acid, chebulinic acid and corilagin. Extract from T. chebula seeds (TCE) has various biological functions. We observed the neuroprotective effects of TCE against ischemic damage in the hippocampal C1 region (CA1) of the gerbil that had received oral administrations of TCE (100?mg/kg) once a day for 7?days before the induction of transient cerebral ischemia. In the TCE-treated ischemia group, neuronal neuclei (a marker for neurons)-positive neurons were distinctively abundant (62% of the sham group) in the CA1 4?days after ischemia-reperfusion (I-R) compared to those (12.2% of the sham group) in the vehicle-treated ischemia group. Four days after I-R TCE treatment markedly decreased the activation of astrocytes and microglia in the ischemic CA1 compared with the vehicle-treated ischemia group. In addition, immunoreactivities of Cu, Zn-superoxide dismutase (SOD1), Mn-superoxide dismutase (SOD2) and brain-derived neurotrophic factor (BDNF) in the CA1 of the TCE-treated ischemia group were much higher than those in the vehicle-ischemia group 4?days after I-R. Protein levels of SOD1, SOD2 and BDNF in the TCE-treated ischemia group were also much higher than those in the vehicle-ischemia group 4?days after I-R. These results indicate that the repeated supplement of TCE protected neurons from ischemic damage induced by transient cerebral ischemia by maintaining SODs and BDNF levels as well as decreasing glial activation. 相似文献
5.
Joon Ha Park Choong Hyun Lee In Hye Kim Ji Hyeon Ahn Jeong-Hwi Cho Bing Chun Yan Jae-Chul Lee Tae Hun Lee Jeong Yeol Seo Jun Hwi Cho Moo-Ho Won Il-Jun Kang 《Neurochemical research》2013,38(12):2640-2649
Glucose is a main energy source for normal brain functions. Glucokinase (GK) plays an important role in glucose metabolism as a glucose sensor, and GK activity is modulated by glucokinase regulatory protein (GKRP). In this study, we examined the changes of GK and GKRP immunoreactivities in the gerbil hippocampus after 5 min of transient global cerebral ischemia. In the sham-operated-group, GK and GKRP immunoreactivities were easily detected in the pyramidal neurons of the stratum pyramidale of the hippocampus. GK and GKRP immunoreactivities in the pyramidal neurons were distinctively decreased in the hippocampal CA1 region (CA), not CA2/3, 3 days after ischemia–reperfusion (I–R). Five days after I–R, GK and GKRP immunoreactivities were hardly detected in the CA1, not CA2/3, pyramidal neurons; however, at this point in time, GK and GKRP immunoreactivities were newly expressed in astrocytes, not microglia, in the ischemic CA1. In brief, GK and GKRP immunoreactivities are changed in pyramidal neurons and newly expressed in astrocytes in the ischemic CA1 after transient cerebral ischemia. These indicate that changes of GK and GKRP expression may be related to the ischemia-induced neuronal damage/death. 相似文献
6.
NADPH derived from glucose-6-phosphate dehydrogenase (G6PD), the rate-limiting enzyme of the pentose phosphate pathway, has been implicated not only to promote reduced glutathione (GSH) but also enhance oxidative stress in specific cellular conditions. In this study, the effects of G6PD antisense oligodeoxynucleotides (AS-ODNs) was examined on the CA1 pyramidal neurons following transient cerebral ischemia. Specifically knockdown of G6PD protein expression in hippocampus CA1 subregion at early reperfusion period (1-24 h) with a strategy to pre-treated G6PD AS-ODNs significantly reduced G6PD activity and NADPH level, an effect correlated with attenuation of NADPH oxidase activation and superoxide anion production. Concomitantly, pre-treatment of G6PD AS-ODNs markedly reduced oxidative DNA damage and the delayed neuronal cell death in rat hippocampal CA1 region induced by global cerebral ischemia. By contrast, knockdown of G6PD protein at late reperfusion period (48-96 h) increased oxidative DNA damage and exacerbated the ischemia-induced neuronal cell death in hippocampal CA1 region, an effect associated with reduced NADPH level and GSH/GSSG ratio. These findings indicate that G6PD not only plays a role in oxidative neuronal damage but also a neuroprotective role during different ischemic reperfusion period. Therefore, G6PD mediated oxidative response and redox regulation in the hippocampal CA1 act as the two sides of the same coin and may represent two potential applications of G6PD during different stage of cerebral ischemic reperfusion. 相似文献
7.
Sohn Y Yoo KY Park OK Kwon SH Lee CH Choi JH Hwang IK Seo JY Cho JH Won MH 《Neurochemical research》2011,36(12):2459-2469
The maintenance of intracellular pH is important in neuronal function. Na+/HCO3
− cotransporter (NBC), a bicarbonate-dependent acid–base transport protein, may contribute to cellular acid–base homeostasis
in pathophysiological processes. We examined the alterations of NBC immunoreactivity and its protein levels in the hippocampal
CA1 region after transient cerebral ischemia in gerbils. In the sham-operated group, moderate NBC immunoreactivity was detected
in CA1 pyramidal neurons, and, 12 h after I/R, the immunoreactivity in the pyramidal neurons was markedly increased over controls.
Three days after I/R, NBC immunoreactivity nearly disappeared in the CA1 pyramidal neurons. However, NBC immunoreactivity
was detected in the non-pyramidal neurons of the ischemic CA1 region at 3 days after I/R. From double immunofluorescence study
with glial markers, NBC immunoreactivity was detected in astrocytes, not in microglia, at 4 days after I/R. NBC protein level
in the CA1 region was significantly increased at 12 h post-ischemia and significantly decreased at 2 days post-ischemia. Thereafter,
NBC protein level was again increased and returned to the level of the sham-operated group at 4 days post-ischemia. On the
other hand, treatment with 4,4′-diisothiocyanatostilbene-2,2′-disulfonate (DIDS), an inorganic anion exchanger blocker including
Cl-bicarbonate exchanger, protected CA1 pyramidal neurons from I/R injury at 4 days post-ischemia. These results indicate
that changes in NBC expressions may play an important role in neuronal damage and astrocytosis induced by transient cerebral
ischemia. 相似文献
8.
Jae-Chul Lee Joon Ha Park Bing Chun Yan In Hye Kim Geum-Sil Cho Dooil Jeoung Young-Geun Kwon Young-Myeong Kim Yun Lyul Lee Hyung-Cheul Shin Moo-Ho Won 《Neurochemical research》2013,38(1):74-81
DNA methylation is a key epigenetic modification of DNA that is catalyzed by DNA methyltransferases (Dnmt). Increasing evidences suggest that DNA methylation in neurons regulates synaptic plasticity as well as neuronal network activity. In the present study, we investigated the changes in DNA methyltransferases 1 (Dnmt1) immunoreactivity and its protein levels in the gerbil hippocampal CA1 region after 5 min of transient global cerebral ischemia. CA1 pyramidal neurons were well stained with NeuN (a neuron-specific soluble nuclear antigen) antibody in the sham-group, Four days after ischemia–reperfusion (I–R), NeuN-positive (+) cells were significantly decreased in the stratum pyramidale (SP) of the CA1 region, and many Fluro-Jade B (a marker for neuronal degeneration)+ cells were observed in the SP. Dnmt1 immunoreactivity was well detected in all the layers of the sham-group. Dnmt1 immunoreactivity was hardly detected only in the stratum pyramidale of the CA1 region from 4 days post-ischemia; however, at these times, Dnmt1 immunoreactivity was newly expressed in GABAergic interneurons or astrocytes in the ischemic CA1 region. In addition, the level of Dnmt1 was lowest at 4 days post-ischemia. In brief, both the Dnmt1 immunoreactivity and protein levels were distinctively decreased in the ischemic CA1 region 4 days after transient cerebral ischemia. These results indicate that the decrease of Dnmt1 expression at 4 days post-ischemia may be related to ischemia-induced delayed neuronal death. 相似文献
9.
Yan BC Park JH Ahn JH Choi JH Yoo KY Lee CH Cho JH Kim SK Lee YL Shin HC Won MH 《Cellular and molecular neurobiology》2012,32(7):1127-1138
It has been reported that young animals are less vulnerable to brain ischemia. In the present study, we compared gliosis in the hippocampal CA1 region of the young gerbil with those in the adult gerbil induced by 5?min of transient cerebral ischemia by immunohistochemistry and western blot for glial cells. We used male gerbils of postnatal month 1 (PM 1) as the young and PM 6 as the adult. Neuronal death in CA1 pyramidal neurons in the adult gerbil occurred at 4?days posti-schemia; the neuronal death in the young gerbil occurred at 7?days post-ischemia. The findings of glial changes in the young gerbil after ischemic damage were distinctively different from those in the adult gerbil. Glial fibrillary acidic protein-immunoreactive astrocytes, ionized calcium-binding adapter molecule (Iba-1), and isolectin B4-immunoreactive microglia in the ischemic CA1 region were activated much later in the young gerbil than in the adult gerbil. In brief, very less gliosis occurred in the hippocampal CA1 region of the young gerbil than in the adult gerbil after transient cerebral ischemia. 相似文献
10.
Cho JH Hwang IK Yoo KY Kim SY Kim DW Kwon YG Choi SY Won MH 《Neurochemistry international》2008,52(4-5):659-668
We examined the intracellular delivery of Pep-1-cargo protein against transient ischemic damage in the hippocampal CA1 region in gerbils. For this study, we introduced green fluorescent protein (GFP) and constructed Pep-1-GFP protein. At 12h after Pep-1-GFP treatment, GFP fluorescence was shown in almost CA1 pyramidal neurons in ischemic animals; in the sham-operated group, GFP fluorescence was shown in a few pyramidal neurons. Next, we confirmed the long-term effects of Pep-1-Cu,Zn-superoxide dismutase 1 (SOD1) against ischemic damage. In behavioral test, locomotor activity was significantly increased in Pep-1- and Pep-1-SOD1-treated groups 1 day after ischemia/reperfusion; the locomotor activity in the Pep-1-treated group was higher than that of the Pep-1-SOD1-treated group. Thereafter, the locomotor activity in both groups was decreased with time. Four days after ischemia/reperfusion, the locomotor activity in the Pep-1-SOD1-treated group was similar to that of the sham group; in the Pep-1-treated group, the activity was lower than that of the sham group. In the histochemical study, the cresyl violet positive neurons in the Pep-1-SOD1-treated group were abundantly detected in the hippocampal CA1 region 5 days after ischemia/reperfusion. In biochemical study, SOD1 protein level and activity in all Pep-1-treated ischemic groups were significantly lower than that of the Pep-1-SOD1-treated group. Our results indicate that Pep-1-cargo fusion proteins can be efficiently delivered into neurons in the ischemic hippocampus, and that Pep-1-SOD1 treatment in ischemic animals show a neuroprotection in the ischemic hippocampus for a long time. 相似文献
11.
AimsA growing number of studies demonstrate that valproic acid (VPA), an anti-convulsant and mood-stabilizing drug, is neuroprotective against various insults. This study investigated whether treatment of ischemic stroke with VPA ameliorated hippocampal cell death and cognitive deficits. Possible mechanisms of action were also investigated.Main methodsGlobal cerebral ischemia was induced to mimic ischemia/reperfusion (I/R) damage. The pyramidal cells within the CA1 field were stained with cresyl violet. Cognitive ability was measured 7 days after I/R using a Morris water maze. The anti-inflammatory effects of VPA on microglia were also investigated by immunohistochemistry. Pro-inflammatory cytokine production was determined using enzyme-linked immunosorbent assays (ELISA). Western blot analysis was performed to determine the levels of acetylated H3, H4 and heat shock protein 70 (HSP70) in extracts from the ischemic hippocampus.Key findingsVPA significantly increased the density of neurons that survived in the CA1 region of the hippocampus on the 7th day after transient global ischemia. VPA ameliorated severe deficiencies in spatial cognitive performance induced by transient global ischemia. Post-insult treatment with VPA also dramatically suppressed the activation of microglia but not astrocytes, reduced the number of microglia, and inhibited other inflammatory markers in the ischemic brain. VPA treatment resulted in a significant increase in levels of acetylated histones H3 and H4 as well as HSP70 in the hippocampus.SignificanceOur results indicated that VPA protected against hippocampal cell loss and cognitive deficits. Treatment with VPA following cerebral ischemia probably involves multiple mechanisms of action, including inhibition of ischemia-induced cerebral inflammation, inhibition of histone deacetylase (HDAC) and induction of HSP. 相似文献
12.
Redd1, also known as RTP801/Dig2/DDIT4, is a stress-induced protein and marked changes of Redd1 expression occurs in response to hypoxia or cerebral ischemia. In the present study, we examined the time-course changes in Redd1 protein expressions in the rat hippocampal CA1 region following chronic cerebral hypoperfusion (CCH) induced by permanent bilateral common carotid arteries occlusion (2VO). Redd1 immunoreactivity in the pyramidal neurons of the hippocampal CA1 region was increased at 7 days after 2VO surgery, and then the immunoreactivity was decreased with time. Especially, very weak Redd1 immunoreactivity was observed in the hippocampal CA1 region at 28 days after 2VO surgery. Western blot analysis showed that Redd1 level in the hippocampal CA1 region was significantly increased at 7 days following CCH and significantly decreased at 28 days after 2VO surgery, compared with that of the sham-operated group. These results indicate that Redd1 expressions is markedly changed in the hippocampal CA1 region following CCH and that change of Redd1 expression may be associated with the CCH-induced neuronal damage in the hippocampal CA1 region. 相似文献
13.
14.
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
15.
16.
17.
1. We investigated the immunohistochemical alterations of BDNF, NGF, HSP 70 and ubiquitin in the hippocampus 1 h to 14 days
after transient cerebral ischemia in gerbils. We also examined the effect of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA)
reductase inhibitor pitavastatin against the changes of BDNF, NGF, HSP 70 and ubiquitin in the hippocampus after cerebral
ischemia in the hippocampus after ischemia.
2. The transient cerebral ischemia was carried out by clamping the carotid arteries with aneurismal clips for 5 min.
3. In the present study, the alteration of HSP 70 and ubiquitin immunoreactivity in the hippocampal CA1 sector was more pronounced
than that of BDNF and NGF immunoreactivity after transient cerebral ischemia. In double-labeled immunostainings, BDNF, NGF
and ubiquitin immunostaining was observed both in GFAP-positive astrocytes and MRF-1-positive microglia in the hippocampal
CA1 sector after ischemia. Furthermore, prophylactic treatment with pitavastatin prevented the damage of neurons with neurotrophic
factor and stress proteins in the hippocampal CA1 sector after ischemia.
4. These findings suggest that the expression of stress protein including HSP 70 and ubiquitin may play a key role in the
protection against the hippocampal CA1 neuronal damage after transient cerebral ischemia in comparison with the expression
of neurotrophic factor such as BDNF and NGF. The present findings also suggest that the glial BDNF, NGF and ubiquitin may
play some role for helping surviving neurons after ischemia. Furthermore, our present study indicates that prophylactic treatment
with pitavastatin can prevent the damage of neurons with neurotrophic factor and stress proteins in the hippocampal CA1 sector
after transient cerebral ischemia. Thus our study provides further valuable information for the pathogenesis after transient
cerebral ischemia.
The first two authors contributed equally 相似文献
18.
Candelario-Jalil E González-Falcón A García-Cabrera M Alvarez D Al-Dalain S Martínez G León OS Springer JE 《Journal of neurochemistry》2003,86(3):545-555
We investigated the relative contribution of COX-1 and/or COX-2 to oxidative damage, prostaglandin E2 (PGE2) production and hippocampal CA1 neuronal loss in a model of 5 min transient global cerebral ischemia in gerbils. Our results revealed a biphasic and significant increase in PGE2 levels after 2 and 24-48 h of reperfusion. The late increase in PGE2 levels (24 h) was more potently reduced by the highly selective COX-2 inhibitor rofecoxib (20 mg/kg) relative to the COX-1 inhibitor valeryl salicylate (20 mg/kg). The delayed rise in COX catalytic activity preceded the onset of histopathological changes in the CA1 subfield of the hippocampus. Post-ischemia treatment with rofecoxib (starting 6 h after restoration of blood flow) significantly reduced measures of oxidative damage (glutathione depletion and lipid peroxidation) seen at 48 h after the initial ischemic episode, indicating that the late increase in COX-2 activity is involved in the delayed occurrence of oxidative damage in the hippocampus after global ischemia. Interestingly, either selective inhibition of COX-2 with rofecoxib or inhibition of COX-1 with valeryl salicylate significantly increased the number of healthy neurons in the hippocampal CA1 sector even when the treatment began 6 h after ischemia. These results provide the first evidence that both COX isoforms are involved in the progression of neuronal damage following global cerebral ischemia, and have important implications for the potential therapeutic use of COX inhibitors in cerebral ischemia. 相似文献
19.
Yan BC Park JH Ahn JH Lee YJ Lee TH Lee CH Cho JH Kim MJ Kim TY Kang IJ Won MH 《Neurochemical research》2012,37(5):1019-1030
In the present study, we compared the immunoreactivities and levels of Trx/prx redox system, thioredoxin 2 (Trx2), thioredoxin reductase 2 (TrxR2) and peroxiredoxin 3 (Prx3), as well as neuronal death in the hippocampal CA1 region between the adult and young gerbil after 5 min of transient cerebral ischemia. At 4 days post-ischemia, pyramidal neurons (about 90%) in the adult stratum pyramidale of the CA1 region showed "delayed neuronal death (DND)"; however, at this time point, few pyramidal neurons showed DND in the young stratum pyramidale. At 7 days post-ischemia, about 56% of pyramidal neurons showed DND in the young stratum pyramidale. The immunoreactivities of all the antioxidants in the young sham-group were similar to those in the adult sham-group. At 4 days post-ischemia, the immunoreactivity of TrxR2, not Trx2 and Prx3 in the adult ischemia-group was dramatically decreased in CA1 pyramidal neurons. At this time point, the immunoreactivities of all the antioxidants in the young ischemia-group were apparently increased compared to the adult ischemia-group. From 7 days pots-ischemia, non-pyramidal cells showed the immunoreactivities of all the antioxidants in the ischemic CA1 region; however, in the young ischemia-groups, the immunoreactivities were much lower than those in the adult ischemia-groups. In brief, our results showed that the immunoreactivities of Trx2, TrxR2 and Prx3 were dramatically increased in CA1 pyramidal neurons of the young ischemia-groups at 4 days post-ischemia compared to those in the adult ischemia-groups induced by transient cerebral ischemia. 相似文献
20.
肢体缺血预处理减少大鼠全脑缺血再灌注诱导的海马CA1区锥体神经元凋亡 总被引:12,自引:0,他引:12
探探讨肢体缺血预处理(limb ischemic preconditioning,LIP)对大鼠全脑缺血再灌注后海马CA1区锥体细胞凋亡的影响。46只大鼠椎动脉凝闭后分为假手术组、肢体缺血组、脑缺血组、LIP组。重复夹闭大鼠双侧股动脉3次(每次10min,间隔10min)作为LIP,之后立即夹闭双侧颈总动脉进行全脑缺血8min后再灌注。DNA凝胶电泳、TUNEL和吖啶橙/溴乙锭(AO/EB)双染技术从生化和形态学方面观察海马神经元凋亡的情况。凝胶电泳显示,脑缺血组出现了凋亡特征性DNA梯状条带,而LIP组无上述条带出现。与脑缺血组比较,LIP可明显减少海马CAI区TUNEL阳性神经元数(17.8±5.8vs 69.8±12,P<0.01)。AO/EB染色也显示LIP可明显减少脑缺血再灌注引起的神经元凋亡。以上结果提示,LIP可抑制脑缺血再灌注后海马神经元的凋亡,进而减轻脑缺血再灌注损伤,提供脑保护作用。 相似文献