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The role of Rho/Rho-kinase pathway and the neuroprotective effects of fasudil in chronic cerebral ischemia 被引量:11
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作者 Ya-yun Yan Xiao-ming Wang +5 位作者 Yan Jiang Han Chen Jin-ting He Jing Mang Yan-kun Shao Zhong-xin Xu 《Neural Regeneration Research》 SCIE CAS CSCD 2015年第9期1441-1449,共9页
The Rho/Rho-kinase signaling pathway plays an important role in cerebral ischemia/reperfusion injury. However, very few studies have examined in detail the changes in the Rho/Rho-kinase signaling pathway in chronic ce... The Rho/Rho-kinase signaling pathway plays an important role in cerebral ischemia/reperfusion injury. However, very few studies have examined in detail the changes in the Rho/Rho-kinase signaling pathway in chronic cerebral ischemia. In this study, rat models of chronic cerebral ischemia were established by permanent bilateral common carotid artery occlusion and intra- gastrically administered 9 mg/kg fasudil, a powerful ROCK inhibitor, for 9 weeks. Morris water maze results showed that cognitive impairment progressively worsened as the cerebral ischemia proceeded. Immunohistochemistry, semi-quantitative RT-PCR and western blot analysis showed that the expression levels of Rho-kinase, its substrate myosin-binding subunit, and its relat- ed protein alpha smooth muscle actin, significantly increased after chronic cerebral ischemia. TUNEL staining showed that chronic cerebral ischemia could lead to an increase in neuronal apoptosis, as well as the expression level of caspase-3 in the frontal cortex of rats subjected to chronic cerebral ischemia. Fasudil treatment alleviated the cognitive impairment in rats with chronic cerebral ischemia, and decreased the expression level of Rho-kinase, myosin-binding subunit and alpha smooth muscle actin. Furthermore, fasudil could regulate cerebral injury by reducing cell apoptosis and decreasing caspase-3 expression in the frontal cortex. These findings demonstrate that fasudil can protect against cognitive impairment induced by chronic cerebral ischemia via the Rho/Rho-kinase signaling pathway and anti-apoptosis mechanism. 展开更多
关键词 nerve regeneration chronic cerebral ischemia FASUDIL RHO-KINASE alpha smooth muscleactin myosin-binding subunit cognitive impairment caspase-3 apoptosis neural regeneration
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Aerobic exercise combined with huwentoxin-I mitigates chronic cerebral ischemia injury 被引量:5
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作者 Hai-feng Mao Jun Xie +6 位作者 Jia-qin Chen Chang-fa Tang Wei Chen Bo-cun Zhou Rui Chen Hong-lin Qu Chu-zu Wu 《Neural Regeneration Research》 SCIE CAS CSCD 2017年第4期596-602,共7页
Ca2+ channel blockers have been shown to protect neurons from ischemia, and aerobic exercise has significant protective effects on a variety of chronic diseases. The present study injected huwentoxin-I (HWTX-I), a ... Ca2+ channel blockers have been shown to protect neurons from ischemia, and aerobic exercise has significant protective effects on a variety of chronic diseases. The present study injected huwentoxin-I (HWTX-I), a spider peptide toxin that blocks Ca2+ channels, into the caudal vein of a chronic cerebral ischemia mouse model, once every 2 days, for a total of 15 injections. During this time, a subgroup of mice was subjected to treadmill exercise for 5 weeks. Results showed amelioration of cortical injury and improved neurological function in mice with chronic cerebral ischemia in the HWTX-I + aerobic exercise group. The combined effects of HWTX I and exercise were superior to HWTX-I or aerobic exercise alone. HWTX-I effectively activated the Notch signal transduction pathway in brain tissue. Aerobic exercise up-regulated synaptophysin mRNA expression. These results demonstrated that aerobic exercise, in combination with HWTX-I, effectively relieved neuronal injury induced by chronic cerebral ischemia via the Notch signaling pathway and promoting synaptic regeneration. 展开更多
关键词 nerve regeneration chronic cerebral ischemia aerobic exercise huwentoxin-I Notch signaling pathway calcium overload neuralregeneration
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Changes of hypoxia-inducible factor-1 signaling and the effect of cilostazol in chronic cerebral ischemia 被引量:5
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作者 Han Chen Aixuan Wei +3 位作者 Jinting He Ming Yu Jing Mang Zhongxin Xu 《Neural Regeneration Research》 SCIE CAS CSCD 2013年第19期1803-1813,共11页
Hypoxiainducible factor1 and its specific target gene heme oxygenase1, are involved in acute cerebral ischemia. However, very few studies have examined in detail the changes in the hy poxiainducible factor1/heme oxyge... Hypoxiainducible factor1 and its specific target gene heme oxygenase1, are involved in acute cerebral ischemia. However, very few studies have examined in detail the changes in the hy poxiainducible factor1/heme oxygenase1 signaling pathway in chronic cerebral ischemia. In this study, a rat model of chronic cerebral ischemia was established by permanent bilateral common carotid artery occlusion, and these rats were treated with intragastric cilostazol (30 mg/kg) for 9 weeks. Morris water maze results showed that cognitive impairment gradually worsened as the cerebral ischemia proceeded. Immunohistochemistry, semiquantitative PCR and western blot analysis showed that hypoxiainducible factorla and heme oxygenase1 expression levels in creased after chronic cerebral ischemia, with hypoxiainducible factorla expression peaking at 3 weeks and heme oxygenase1 expression peaking at 6 weeks. These results suggest that the elevated levels of hypoxiainducible factorla may upregulate heine oxygenase1 expression fol lowing chronic cerebral ischemia and that the hypoxiainducible factor1/heme oxygenase1 sig naling pathway is involved in the development of cognitive impairment induced by chronic cerebral ischemia. Cilostazol treatment alleviated the cognitive impairment in rats with chronic cerebral ischemia, decreased hypoxiainducible factorla and heme oxygenase1 expression levels, and reduced apoptosis in the frontal cortex. These findings demonstrate that cilostazol can protect against cognitive impairment induced by chronic cerebral ischemic injury through an antiapoptotic mechanism. 展开更多
关键词 neural regeneration chronic cerebral ischemia cognitive impairment hypoxia-inducible factor-I hemeoxygenase-1 CILOSTAZOL apoptosis grants-supported paper NEUROREGENERATION
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Neuroprotective effects of kaempferol against 2VO-induced chronic cerebral ischemia in rats 被引量:3
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作者 ZHANG Jun CHENG Xiao +5 位作者 YANG Huan YANG Yin-lin ZHAO Ting-kun WANG Qi WANG Yue-hua DU Guan-hua 《中国药理学与毒理学杂志》 CAS CSCD 北大核心 2016年第10期1028-1029,共2页
OBJECTIVE To investigate the effects of kaempferol(KAE)on chronic cerebral ischemia in rats.METHODS Chronic cerebral ischemia was induced in rats by permanent occlusion of bilateral common carotid arteries(2VO).Then,t... OBJECTIVE To investigate the effects of kaempferol(KAE)on chronic cerebral ischemia in rats.METHODS Chronic cerebral ischemia was induced in rats by permanent occlusion of bilateral common carotid arteries(2VO).Then,the rats with chronic cerebral ischemia were randomly divied into three groups:model group,KAE 10 and 30 mg·kg-1group.Another group rats without occlusion of common carotid arteries were used as the sham-operation group.Memory behavior was investigated by Morris water maze test.Prehensile ability was investigated by prehensile traction test.The structure of hippocampus and cortex neurons was observed with Nissel staining.In addition,the SOD activity and MDA content in brain tissue were determined.The DJ-1protein level was determined by Western blotting.RESULTS KAE 10 and 30 mg·kg-1could significantly improve cognitive impairment and prehensile traction ability(P<0.01)induced by chronic cerebral ischemia in rats.The results of the pathological analysis also suggested that KAE could ameliorate the pathological damage induced by chronic cerebral ischemia.In addition,KAE 30 mg·kg-1significantly increased the activity of SOD(P<0.05),but had no effect on the content of MDA in rat brain tissue.Western-blotting confirmed that KAE 10 and30 mg·kg-1could increase the expression of anti-oxidation proteins DJ-1 in hippocampus(P<0.01).CONCLUSION KAE may attenuate the chronic cerebral ischemic injury in rats. 展开更多
关键词 KAEMPFEROL chronic cerebral ischemia occlusion of bilateral common carotid arteries
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Effects of chronic peripheral pretreatment with an angiotensin II type-1 receptor blocker on apoptosis-related molecules in rats with cerebral ischemia/reperfusion injury 被引量:3
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作者 Jingping Shi Jingde Dong Jie Lu Yingdong Zhang 《Neural Regeneration Research》 SCIE CAS CSCD 2010年第15期1150-1155,共6页
Chronic systemic treatment with blockers of angiotensin II type-1 (AT1) receptors inhibits ischemia-induced apoptosis and reduces ischemic neuronal damage. However, the molecular mechanisms of AT1 receptor blockers ... Chronic systemic treatment with blockers of angiotensin II type-1 (AT1) receptors inhibits ischemia-induced apoptosis and reduces ischemic neuronal damage. However, the molecular mechanisms of AT1 receptor blockers in modulating neuronal apoptosis remain poorly understood. Pretreatment with irbesartan significantly suppressed cell apoptosis at 1-7 days following cerebral ischemia/reperfusion, increased levels of brain-derived neurotrophic factor, and elevated the ratios of Bcl-2/Bax and phosphorylated cyclic adenosine monophosphate response element-binding protein (pCREB)/CREB in the ischemic cortex at 1 day after reperfusion, as well as suppressing caspase-3 activation. Cerebral ischemia increased the mRNA expression of AT1 and AT2 receptors in the ischemic cortex, whereas irbesartan blocked this increase in AT1 expression but potentiated the expression of AT2. Therefore, this AT1 receptor blocker was neuroprotective by increasing the ratios of Bcl-2/Bax and pCREB/CREB, increasing brain-derived neurotrophic factor levels, inhibiting caspase-3 activation, and modulating AT receptor expression. 展开更多
关键词 angiotensin II cerebral ischemia RECEPTOR APOPTOSIS brain-derived neurotrophic factor brain injury neural regeneration
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Estrogen intervention in microvascular morphology and choline acetyltransferase expression in rat hippocampal neurons in chronic cerebral ischemia 被引量:1
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作者 Zhenjun Yang Hongwei Yan +2 位作者 Guomin Zhang Zhihong Chen Jingfeng xue 《Neural Regeneration Research》 SCIE CAS CSCD 2011年第17期1285-1290,共6页
We observed dynamic changes in microvessels and a protective effect of estrogen on chronic cerebral ischemia ovariectomized rat models established through permanent occlusion of bilateral carotid arteries at 7, 14 and... We observed dynamic changes in microvessels and a protective effect of estrogen on chronic cerebral ischemia ovariectomized rat models established through permanent occlusion of bilateral carotid arteries at 7, 14 and 21 days. The results revealed that estrogen improved microvasculature in the hippocampus of chronic cerebral ischemic rats, upregulated Bcl-2 protein expression, downregulated Bax protein expression, increased choline acetyltransferase expression in hippocampal cholinergic neurons, and suppressed hippocampal neuronal apoptosis. These findings indicate that estrogen can protect hippocampal neurons in rats with chronic cerebral ischemia. 展开更多
关键词 ESTROGEN chronic cerebral ischemia HIPPOCAMPUS MICROVASCULATURE Bcl-2 BAX choline acetyltransferase neural regeneration
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Curcumin alters expression of glial fibrillary acidic protein and nestin following chronic cerebral ischemia 被引量:1
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作者 Peng Zhang 《Neural Regeneration Research》 SCIE CAS CSCD 2011年第9期651-655,共5页
Astrocytes can alter their appearance and become reactive following chronic cerebral ischemia. In the present study, a rat model of chronic cerebral ischemia was treated with 50 and 100 mg/kg curcumin. Results showed ... Astrocytes can alter their appearance and become reactive following chronic cerebral ischemia. In the present study, a rat model of chronic cerebral ischemia was treated with 50 and 100 mg/kg curcumin. Results showed that pathological changes of neuronal injury in hippocampal CA1 area of rats induced by chronic cerebral ischemia were attenuated, as well as upregulated expression of glial fibriliary acidic protein and nestin, in a dose-dependent manner. 展开更多
关键词 CURCUMIN chronic cerebral ischemia glial fibrillary acidic protein NESTIN NIDOGEN permanent occlusion of bilateral common carotid arteries
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Effect of propofol on brain-derived neurotrophic factor and tyrosine kinase receptor B in the hippocampus of aged rats with chronic cerebral ischemia 被引量:1
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作者 Gang Chen Qiang Fu Jiangbei Cao Weidong Mi 《Neural Regeneration Research》 SCIE CAS CSCD 2012年第21期1645-1649,共5页
We intraperitoneally injected 10 and 50 mg/kg of propofol for 7 consecutive days to treat a rat model of chronic cerebral ischemia. A low-dose of propofol promoted the expression of brain-derived neurotrophic factor, ... We intraperitoneally injected 10 and 50 mg/kg of propofol for 7 consecutive days to treat a rat model of chronic cerebral ischemia. A low-dose of propofol promoted the expression of brain-derived neurotrophic factor, tyrosine kinase receptor B, phosphorylated cAMP response element binding protein, and cAMP in the hippocampus of aged rats with chronic cerebral ischemia, but a high-dose of propofol inhibited their expression. Results indicated that the protective effect of propofol against cerebral ischemia in aged rats is related to changes in the expression of brain-derived neurotrophic factor and tyrosine kinase receptor B in the hippocampus, and that the cAMP-cAMP responsive element binding protein pathway is involved in the regulatory effect of propofol on brain-derived neurotrophic factor expression. 展开更多
关键词 PROPOFOL chronic cerebral ischemia aged brain-derived neurotrophic factor tyrosine kinasereceptor B cAMP-cAMP responsive element binding protein neural regeneration
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Bumetanide promotes neural precursor cell regeneration and dendritic development in the hippocampal dentate gyrus in the chronic stage of cerebral ischemia 被引量:1
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作者 Wang-shu Xu Xuan Sun +4 位作者 Cheng-guang Song Xiao-peng Mu Wen-ping Ma Xing-hu Zhang Chuan-sheng Zhao 《Neural Regeneration Research》 SCIE CAS CSCD 2016年第5期745-751,共7页
Bumetanide has been shown to lessen cerebral edema and reduce the infarct area in the acute stage of cerebral ischemia. Few studies focus on the effects of bumetanide on neuroprotection and neurogenesis in the chronic... Bumetanide has been shown to lessen cerebral edema and reduce the infarct area in the acute stage of cerebral ischemia. Few studies focus on the effects of bumetanide on neuroprotection and neurogenesis in the chronic stage of cerebral ischemia. We established a rat model of cerebral ischemia by injecting endothelin-1 in the left cortical motor area and left corpus striatum. Seven days later, bumetanide 200 μg/kg/day was injected into the lateral ventricle for 21 consecutive days with a mini-osmotic pump. Results demonstrated that the number of neuroblasts cells and the total length of dendrites increased, escape latency reduced, and the number of platform crossings increased in the rat hippocampal dentate gyrus in the chronic stage of cerebral ischemia. These findings suggest that bumetanide promoted neural precursor cell regeneration, dendritic development and the recovery of cognitive function, and protected brain tissue in the chronic stage of ischemia. 展开更多
关键词 nerve regeneration cerebral ischemia BUMETANIDE Na+-K+-2Cl- cotransporter 1 hippocampal dentate gyrus neurogenesis neuralprecursor cells dendritic development cognitive function neural regeneration
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Intercellular adhesion molecule-1 expression in the hippocampal CA1 region of hyperlipidemic rats with chronic cerebral ischemia
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作者 Yingying Cheng Ying Zhang +1 位作者 Hongmei Song Jiachun Feng 《Neural Regeneration Research》 SCIE CAS CSCD 2012年第17期1312-1317,共6页
Chronic cerebral ischemia is a pathological process in many cerebrovascular diseases and it is induced by long-term hypedipidemia, hypertension and diabetes mellitus. After being fed a high-fat diet for 4 weeks, rats ... Chronic cerebral ischemia is a pathological process in many cerebrovascular diseases and it is induced by long-term hypedipidemia, hypertension and diabetes mellitus. After being fed a high-fat diet for 4 weeks, rats were subjected to permanent occlusion of bilateral common carotid arteries to establish rat models of chronic cerebral ischemia with hypedipiclemia. Intercellular adhesion molecule-1 expression in rat hippocampal CA1 region was determined to better understand the mechanism underlying the effects of hypedipidemia on chronic cerebral ischemia. Water maze test results showed that the cognitive function of rats with hyperlipidemia or chronic cerebral ischemia, particulady in rats with hypedipidemia combined with chronic cerebral ischemia, gradually decreased between 1 and 4 months after occlusion of the bilateral common carotid arteries. This correlated with pathological changes in the hippocampal CA1 region as detected by hematoxylin-eosin staining. Immunohistochemical staining showed that intercellular adhesion molecule-1 expression in the hippocampal CA1 region was noticeably increased in rats with hyperlipidemia or chronic cerebral ischemia, in particular in rats with hyperlipidemia combined with chronic cerebral ischemia. These findings suggest that hyperlipidemia aggravates chronic cerebral ischemia-induced neurological damage and cognitive impairment in the rat hippocampal CA1 region which may be mediated, at least in part, by up-regulated expression of intercellular adhesion molecule-l. 展开更多
关键词 HYPERLIPIDEMIA chronic cerebral ischemia intercellular adhesion molecule-I HIPPOCAMPUS CA1 water maze test cognitive function neural regeneration
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Hippocampal mitochondrial cytochrome C oxidase activity and gene expression in a rat model of chronic cerebral ischemia
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作者 Qing Zhao Yingli Zhang +4 位作者 Mingming Zhao Yu Wang Ming Ma Xinquan Gu Xia Cao 《Neural Regeneration Research》 SCIE CAS CSCD 2011年第32期2527-2531,共5页
The present study established a rat model of chronic cerebral ischemia using bilateral common carotid artery permanent ligation to analyze cytochrome C oxidase activity and mRNA expression in hippocampal mitochondria.... The present study established a rat model of chronic cerebral ischemia using bilateral common carotid artery permanent ligation to analyze cytochrome C oxidase activity and mRNA expression in hippocampal mitochondria. Results showed significantly decreased cytochrome C oxidase activity and cytochrome C oxidase II mRNA expression with prolonged ischemia time. Further analysis revealed five mitochondrial cytochrome C oxidase II gene mutations, two newly generated mutations, and four absent mutational sites at 1 month after cerebral ischemia, as well as three mitochondrial cytochrome C oxidase III gene mutations, including two newly generating mutations, and one disappeared mutational site at 1 month after cerebral ischemia. Results demonstrated that decreased cytochrome C oxidase gene expression and mutations, as well as decreased cytochrome C oxidase activity, resulting in energy dysmetabolism, which has been shown to be involved in the DatholoQical Process of ischemic brain iniurv. 展开更多
关键词 cerebral ischemia cytochrome C oxidase gene mutation HIPPOCAMPUS MITOCHONDRION neural regeneration
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Effects of CXCR7-neutralizing antibody on neurogenesis in the hippocampal dentate gyrus and cognitive function in the chronic phase of cerebral ischemia 被引量:3
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作者 Bing-Chao Dong Mei-Xuan Li +6 位作者 Xiao-Yin Wang Xi Cheng Yu Wang Ting Xiao Jukka Jolkkonen Chuan-Sheng Zhao Shan-Shan Zhao 《Neural Regeneration Research》 SCIE CAS CSCD 2020年第6期1079-1085,共7页
Stromal cell-derived factor-1 and its receptor CXCR4 are essential regulators of the neurogenesis that occurs in the adult hippocampal dentate gyrus.However,the effects of CXCR7,a new atypical receptor of stromal cell... Stromal cell-derived factor-1 and its receptor CXCR4 are essential regulators of the neurogenesis that occurs in the adult hippocampal dentate gyrus.However,the effects of CXCR7,a new atypical receptor of stromal cell-derived factor-1,on hippocampal neurogenesis after a stroke remain largely unknown.Our study is the first to investigate the effect of a CXCR7-neutralizing antibody on neurogenesis in the dentate gyrus and the associated recovery of cognitive function of rats in the chronic stage of cerebral ischemia.The rats were randomly divided into sham,sham+anti-CXCR7,ischemia and ischemia+anti-CXCR7 groups.Endothelin-1 was injected in the ipsilateral motor cortex and striatum to induce focal cerebral ischemia.Sham group rats were injected with saline instead of endothelin-1 via intracranial injection.Both sham and ischemic rats were treated with intraventricular infusions of CXCR7-neutralizing antibodies for 6 days 1 week after surgery.Immunofluorescence staining with doublecortin,a marker for neuronal precursors,was performed to assess the neurogenesis in the dentate gyrus.We found that anti-CXCR7 antibody infusion enhanced the proliferation and dendritic development of doublecortin-labeled cells in the dentate gyrus in both ischemic and sham-operated rats.Spatial learning and memory functions were assessed by Morris water maze tests 30-32 days after ischemia.CXCR7-neutralizing antibody treatment significantly reduced the escape latency of the spatial navigation trial and increased the time spent in the target quadrant of spatial probe trial in animals that received ischemic insult,but not in sham operated rats.These results suggest that CXCR7-neutralizing antibody enhances the neurogenesis in the dentate gyrus and improves the cognitive function after cerebral ischemia in rats.All animal experimental protocols and procedures were approved by the Institutional Animal Care and Use Committee of China Medical University(CMU16089 R)on December 8,2016. 展开更多
关键词 cerebral ischemia cognitive function CXCR7 dendritic development DENTATE GYRUS DOUBLECORTIN NEUROGENESIS NEUTRALIZING antibody stroke stromal cell-derived factor-1
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Treatment with β-sitosterol ameliorates the effects of cerebral ischemia/reperfusion injury by suppressing cholesterol overload, endoplasmic reticulum stress, and apoptosis 被引量:2
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作者 Xiuling Tang Tao Yan +8 位作者 Saiying Wang Qingqing Liu Qi Yang Yongqiang Zhang Yujiao Li Yumei Wu Shuibing Liu Yulong Ma Le Yang 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第3期642-649,共8页
β-Sitosterol is a type of phytosterol that occurs naturally in plants.Previous studies have shown that it has anti-oxidant,anti-hyperlipidemic,anti-inflammatory,immunomodulatory,and anti-tumor effects,but it is unkno... β-Sitosterol is a type of phytosterol that occurs naturally in plants.Previous studies have shown that it has anti-oxidant,anti-hyperlipidemic,anti-inflammatory,immunomodulatory,and anti-tumor effects,but it is unknown whetherβ-sitosterol treatment reduces the effects of ischemic stroke.Here we found that,in a mouse model of ischemic stroke induced by middle cerebral artery occlusion,β-sitosterol reduced the volume of cerebral infarction and brain edema,reduced neuronal apoptosis in brain tissue,and alleviated neurological dysfunction;moreover,β-sitosterol increased the activity of oxygen-and glucose-deprived cerebral cortex neurons and reduced apoptosis.Further investigation showed that the neuroprotective effects ofβ-sitosterol may be related to inhibition of endoplasmic reticulum stress caused by intracellular cholesterol accumulation after ischemic stroke.In addition,β-sitosterol showed high affinity for NPC1L1,a key transporter of cholesterol,and antagonized its activity.In conclusion,β-sitosterol may help treat ischemic stroke by inhibiting neuronal intracellular cholesterol overload/endoplasmic reticulum stress/apoptosis signaling pathways. 展开更多
关键词 APOPTOSIS blood-brain barrier Β-SITOSTEROL cerebral ischemia/reperfusion injury cholesterol overload cholesterol transport endoplasmic reticulum stress ischemic stroke molecular docking NPC1L1
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Cav3.2 channel regulates cerebral ischemia/reperfusion injury:a promising target for intervention 被引量:1
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作者 Feibiao Dai Chengyun Hu +7 位作者 Xue Li Zhetao Zhang Hongtao Wang Wanjun Zhou Jiawu Wang Qingtian Geng Yongfei Dong Chaoliang Tang 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第11期2480-2487,共8页
Calcium influx into neurons triggers neuronal death during cerebral ischemia/reperfusion injury.Various calcium channels are involved in cerebral ischemia/reperfusion injury.Cav3.2 channel is a main subtype of T-type ... Calcium influx into neurons triggers neuronal death during cerebral ischemia/reperfusion injury.Various calcium channels are involved in cerebral ischemia/reperfusion injury.Cav3.2 channel is a main subtype of T-type calcium channels.T-type calcium channel blockers,such as pimozide and mibefradil,have been shown to prevent cerebral ischemia/reperfusion injury-induced brain injury.However,the role of Cav3.2 channels in cerebral ischemia/reperfusion injury remains unclear.Here,in vitro and in vivo models of cerebral ischemia/reperfusion injury were established using middle cerebral artery occlusion in mice and high glucose hypoxia/reoxygenation exposure in primary hippocampal neurons.The results showed that Cav3.2 expression was significantly upregulated in injured hippocampal tissue and primary hippocampal neurons.We further established a Cav3.2 gene-knockout mouse model of cerebral ischemia/reperfusion injury.Cav3.2 knockout markedly reduced infarct volume and brain water content,and alleviated neurological dysfunction after cerebral ischemia/reperfusion injury.Additionally,Cav3.2 knockout attenuated cerebral ischemia/reperfusion injury-induced oxidative stress,inflammatory response,and neuronal apoptosis.In the hippocampus of Cav3.2-knockout mice,calcineurin overexpression offset the beneficial effect of Cav3.2 knockout after cerebral ischemia/reperfusion injury.These findings suggest that the neuroprotective function of Cav3.2 knockout is mediated by calcineurin/nuclear factor of activated T cells 3 signaling.Findings from this study suggest that Cav3.2 could be a promising target for treatment of cerebral ischemia/reperfusion injury. 展开更多
关键词 CALCINEURIN Cav3.2 channel cerebral ischemia/reperfusion hippocampus HYPOXIA/REOXYGENATION inflammatory response nuclear factor of activated T cells 3 oxidative stress primary hippocampal neurons stroke
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Activation of GABAB receptors alleviates depressive-like behavior induced by chronic cerebral ischemia via upredulation of BDNF in rats
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《中国药理学通报》 CAS CSCD 北大核心 2015年第B11期77-78,共2页
Aim To investigate the mechanisms underlying depressive-like behavior induced by chronic cerebral is- chemia in rats. Methods In the present study, a chronic cerebral hypoperfusion model was established by perma- 2VO... Aim To investigate the mechanisms underlying depressive-like behavior induced by chronic cerebral is- chemia in rats. Methods In the present study, a chronic cerebral hypoperfusion model was established by perma- 2VO) in rats. Two weeks after 2VO, GAB- nent bilateral common carotid arteries occlusion (two-vessel occlusion, AB receptor agonist baclofen (25 mg · kg^-1 . d^-1 i p ) was administrated for 21 days. The FST was performed to evaluate depressive-like behavior in which the immobility time was recorded. In addition, the expression of brain derived neurotrophic factor (BDNF) in hippocampal CA1 was measured by Western blot. Results The immobility time of 2VO group was significantly prolonged and the expression of BDNF was decreased by 28.95% compared with sham group. After activation of GABAB receptors by baclofen, the immobility time was significantly reduced and the expression of BDNF was increased by 47.91% compared with 2VO group. Conclusion 2VO induced ob- vious depressive-like behavior in rats. Activation of GABAB receptors alleviates the depressive-like behavior in- duced by chronic cerebral ischemia via upredulation of BDNF in hippocampal CA1 in rats. 展开更多
关键词 GABAB RECEPTORS BACLOFEN depressive-like behavior chronic cerebral ischemia BDNF hippocampalCA1
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Lactiplantibacillus plantarum AR113 alleviates microbiota dysbiosis of tongue coating and cerebral ischemia/reperfusion injury in rat
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作者 Zhiqiang Xiong Gang Liu +5 位作者 Ling Fang Xiuming Li Yongjun Xia Guangqiang Wang Xin Song Lianzhong Ai 《Food Science and Human Wellness》 SCIE CAS CSCD 2024年第4期2132-2140,共9页
Stroke is one of the leading causes of death and disability worldwide.However,information on stroke-related tongue coating microbiome(TCM)is limited,and whether TCM modulation could benefit for stroke prevention and r... Stroke is one of the leading causes of death and disability worldwide.However,information on stroke-related tongue coating microbiome(TCM)is limited,and whether TCM modulation could benefit for stroke prevention and rehabilitation is unknown.Here,TCM from stroke patients(SP)was characterized using molecular techniques.The occurrence of stroke resulted in TCM dysbiosis with significantly reduced species richness and diversity.The abundance of Prevotella,Leptotrichia,Actinomyces,Alloprevotella,Haemophilus,and TM7_[G-1]were greatly reduced,but common infection Streptococcus and Pseudomonas were remarkably increased.Furthermore,an antioxidative probiotic Lactiplantibacillus plantarum AR113 was used for TCM intervention in stroke rats with cerebral ischemia/reperfusion(I/R).AR113 partly restored I/R induced change of TCM and gut microbiota with significantly improved neurological deficit,relieved histopathologic change,increased activities of antioxidant enzymes,and decreased contents of oxidative stress biomarkers.Moreover,the gene expression of antioxidant-related proteins and apoptosis-related factors heme oxygenase-1(HO-1),superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),nuclear factor erythroid 2-related factor 2(Nrf2),NAD(P)H:quinone oxidoreductase-1(NQO-1),and Bcl-2 was significantly increased,but cytochrome C,cleaved caspase-3,and Bax were markedly decreased in the brain by AR113 treatment.The results suggested that AR113 could ameliorate cerebral I/R injury through antioxidation and anti-apoptosis pathways,and AR113 intervention of TCM may have the application potential for stroke prevention and control. 展开更多
关键词 Stroke cerebral ischemia/reperfusion Tongue coating Lactiplantibacillus plantarum AR113 Probiotic intervention
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Xiao-Xu-Ming decoction protects against chronic cerebral ischemia injury in rats and profile of differentially expression proteins analysis in hippocampus
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作者 Yue-hua WANG Yin-lin YANG +4 位作者 Xiao CHENG Jun ZHANG Wan LI Wei-han LI Guan-hua DU 《中国药理学与毒理学杂志》 CAS CSCD 北大核心 2018年第4期310-311,共2页
OBJECTIVE Vascular dementia(VD) refers to a progressive decline in memory and cognitive function caused by chronic cerebral ischemia.2-Vessels occlusion(2-VO) has been widely used as a model of VD.Xiao-Xu-Ming decocti... OBJECTIVE Vascular dementia(VD) refers to a progressive decline in memory and cognitive function caused by chronic cerebral ischemia.2-Vessels occlusion(2-VO) has been widely used as a model of VD.Xiao-Xu-Ming decoction,a well-known traditional Chinese medicine prescrip.tion,has been widely used to treat stroke and sequelae of stroke.The present study was to investigate the mechanism of Xiao-Xu-Ming decoction(XXM) against chronic cerebral ischemia injury in rats.METHODS After XXM treatment,rats were performed a memory testing with Morris water maze and motor ability testing using prehensile test and inclined screen test.Neuronal plasticity was observed by immunofluorescent staining with MAP2 antibody.Differentially expressed proteins of rat hippocampus were analyzed by Label-free quantitative proteomics.RESULTS XXM significantly alleviated 2-VOinduced learning and memory deficits,motor ability dysfunction,and neuronal plasticity injury in rats.The mechanism might be involved in up-regulation of 39 proteins and down-regulation of 13 proteins in the hippocampus of rats after XXM treatment vs 2-VO group rats.Gene ontology and pathway analysis showed that the regulated proteins are mainly involved in oxidation reduction process,intracellular signaling cascade process,and protein catabolic process,etc.The signal pathways are mainly involved in ubiquitin mediated proteolysis and phosphatidylinositol signaling system.CONCLUSION Current findings provide new insights into the molecular mechanisms of XXM on chronic cerebral ischemia. 展开更多
关键词 血管性痴呆 慢性脑缺血 治疗方法 临床分析
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Endoplasmic reticulum stress and autophagy in cerebral ischemia/reperfusion injury:PERK as a potential target for intervention
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作者 Ju Zheng Yixin Li +8 位作者 Ting Zhang Yanlin Fu Peiyan Long Xiao Gao Zhengwei Wang Zhizhong Guan Xiaolan Qi Wei Hong Yan Xiao 《Neural Regeneration Research》 SCIE CAS 2025年第5期1455-1466,共12页
Several studies have shown that activation of unfolded protein response and endoplasmic reticulum(ER)stress plays a crucial role in severe cerebral ischemia/reperfusion injury.Autophagy occurs within hours after cereb... Several studies have shown that activation of unfolded protein response and endoplasmic reticulum(ER)stress plays a crucial role in severe cerebral ischemia/reperfusion injury.Autophagy occurs within hours after cerebral ischemia,but the relationship between ER stress and autophagy remains unclear.In this study,we established experimental models using oxygen-glucose deprivation/reoxygenation in PC12 cells and primary neurons to simulate cerebral ischemia/reperfusion injury.We found that prolongation of oxygen-glucose deprivation activated the ER stress pathway protein kinase-like endoplasmic reticulum kinase(PERK)/eukaryotic translation initiation factor 2 subunit alpha(e IF2α)-activating transcription factor 4(ATF4)-C/EBP homologous protein(CHOP),increased neuronal apoptosis,and induced autophagy.Furthermore,inhibition of ER stress using inhibitors or by si RNA knockdown of the PERK gene significantly attenuated excessive autophagy and neuronal apoptosis,indicating an interaction between autophagy and ER stress and suggesting PERK as an essential target for regulating autophagy.Blocking autophagy with chloroquine exacerbated ER stress-induced apoptosis,indicating that normal levels of autophagy play a protective role in neuronal injury following cerebral ischemia/reperfusion injury.Findings from this study indicate that cerebral ischemia/reperfusion injury can trigger neuronal ER stress and promote autophagy,and suggest that PERK is a possible target for inhibiting excessive autophagy in cerebral ischemia/reperfusion injury. 展开更多
关键词 apoptosis ATF4 AUTOPHAGY C/EBP homologous protein cerebral ischemia/reperfusion injury EIF2Α endoplasmic reticulum stress PERK
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A matrix metalloproteinase-responsive hydrogel system controls angiogenic peptide release for repair of cerebral ischemia/reperfusion injury
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作者 Qi Liu Jianye Xie +5 位作者 Runxue Zhou Jin Deng Weihong Nie Shuwei Sun Haiping Wang Chunying Shi 《Neural Regeneration Research》 SCIE CAS 2025年第2期503-517,共15页
Vascular endothelial growth factor and its mimic peptide KLTWQELYQLKYKGI(QK)are widely used as the most potent angiogenic factors for the treatment of multiple ischemic diseases.However,conventional topical drug deliv... Vascular endothelial growth factor and its mimic peptide KLTWQELYQLKYKGI(QK)are widely used as the most potent angiogenic factors for the treatment of multiple ischemic diseases.However,conventional topical drug delivery often results in a burst release of the drug,leading to transient retention(inefficacy)and undesirable diffusion(toxicity)in vivo.Therefore,a drug delivery system that responds to changes in the microenvironment of tissue regeneration and controls vascular endothelial growth factor release is crucial to improve the treatment of ischemic stroke.Matrix metalloproteinase-2(MMP-2)is gradually upregulated after cerebral ischemia.Herein,vascular endothelial growth factor mimic peptide QK was self-assembled with MMP-2-cleaved peptide PLGLAG(TIMP)and customizable peptide amphiphilic(PA)molecules to construct nanofiber hydrogel PA-TIMP-QK.PA-TIMP-QK was found to control the delivery of QK by MMP-2 upregulation after cerebral ischemia/reperfusion and had a similar biological activity with vascular endothelial growth factor in vitro.The results indicated that PA-TIMP-QK promoted neuronal survival,restored local blood circulation,reduced blood-brain barrier permeability,and restored motor function.These findings suggest that the self-assembling nanofiber hydrogel PA-TIMP-QK may provide an intelligent drug delivery system that responds to the microenvironment and promotes regeneration and repair after cerebral ischemia/reperfusion injury. 展开更多
关键词 angiogenesis biomaterial blood-brain barrier cerebral ischemia/reperfusion injury control release drug delivery inflammation QK peptides matrix metalloproteinase-2 NEUROPROTECTION self-assembling nanofiber hydrogel
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Neuroprotective effects of saffron on chronic focal cerebral ischemia through inhibiting glial scar formation in rats
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作者 Yi-lu YE Rou-xin WANG +4 位作者 Si-qi YAO Ze-kang FANG Kai ZHONG Qi ZHANG Yue-ping YU 《中国药理学与毒理学杂志》 CAS CSCD 北大核心 2018年第4期326-326,共1页
OBJECTIVE To explore the neuro-protective effects of saffron(Crocus satius L.) on chronic focal cerebral ischemia in rats.METHODS SD rats were randomly divided into 6 groups:sham control group,MCAO group,edaravone gro... OBJECTIVE To explore the neuro-protective effects of saffron(Crocus satius L.) on chronic focal cerebral ischemia in rats.METHODS SD rats were randomly divided into 6 groups:sham control group,MCAO group,edaravone group and saffron 30,100,300 mg·kg^(-1) groups.Focal cerebral ischemia was induced by middle cerebral artery occlusion(MCAO).Saffron was administered orally by once daily from 2 h to 42 d after ischemia.At 42 d after cerebral ischemia,neurological deficit score,spontaneous activity test,elevated plus maze test,marble burying test and novel objective recognition test were used to evaluate the effects of saffron on the behevioural change.Infarct volume,survival neuron density,activated astrocyte number,and the thickness of glial scar were also detected.GFAP expression and inflammatory cytokine contents in ischemic peripheral region were detected by Western blot and ELISA,separately.RESULTS Saffron(100,300 mg·kg^(-1)) improved the body weight decrease,neurological deficit and spontaneous activity.Saffron(30-300 mg · kg^(-1)) increased the traveled distance ratio and total time in open arm,decreased the buried marble number,which indicated that saffron could ameliorate anxiety-and depression-like behaviors.Saffron(100,300 mg·kg^(-1)) improved the learning and memory function,which manifested by increased discrimination ratio(DR) and discrim.ination index(DI) in T2 test.The results of toluidine blue found saffron treatment(100,300 mg · kg^(-1))decreased the infarct volume and increased the neuron density in cortex and hippocampal.The activated astrocyte number,the thickness of glial scar and GFAP expression in ischemic peripheral region decreased after saffron.Saffron(100,300 mg · kg^(-1)) decreased the contents of IL-6 and IL-1β,increased the content of IL-10 in ischemic peripheral region.CONCLUSION Saffron exerted neuro-protective effects on chronic focal cerebral ischemia,which could be related with inhibiting the activation of astrocyte and glial scar,following with the decrease of inflammatory reaction. 展开更多
关键词 藏红花 脑缺血 治疗方法 临床分析
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