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The critical role of the endolysosomal system in cerebral ischemia

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Neural Regeneration Research 2023年第5期18卷 983-990页

作者： Hui-Yi Zhang Ye Tian Han-Yan Shi Ya Cai Ying Xu Department of Anesthesiology Shengjing Hospital of China Medical UniversityShenyangLiaoning ProvinceChina Department of Orthopedics Shengjing Hospital of China Medical UniversityShenyangLiaoning ProvinceChina

Cerebral ischemia is a serious disease that triggers sequential pathological mechanisms, leading to significant morbidity and mortality. Although most studies to date have typically focused on the lysosome, a single organelle, current evidence supports that the function of lysosomes cannot be separated from that of the endolysosomal system as a whole. The associated membrane fusion functions of this system play a crucial role in the biodegradation of cerebral ischemia-related products. Here, we review the regulation of and the changes that occur in the endolysosomal system after cerebral ischemia, focusing on the latest research progress on membrane fusion function. Numerous proteins, including N-ethylmaleimide-sensitive factor and lysosomal potassium channel transmembrane protein 175, regulate the function of this system. However, these proteins are abnormally expressed after cerebral ischemic injury, which disrupts the normal fusion function of membranes within the endolysosomal system and that between autophagosomes and lysosomes. This results in impaired “maturation” of the endolysosomal system and the collapse of energy metabolism balance and protein homeostasis maintained by the autophagy-lysosomal pathway. Autophagy is the final step in the endolysosomal pathway and contributes to maintaining the dynamic balance of the system. The process of autophagosome-lysosome fusion is a necessary part of autophagy and plays a crucial role in maintaining energy homeostasis and clearing aging proteins. We believe that, in cerebral ischemic injury, the endolysosomal system should be considered as a whole rather than focusing on the lysosome. Understanding how this dynamic system is regulated will provide new ideas for the treatment of cerebral ischemia.

关键词： autophagy biodegradation brain injury chaperone-mediated autophagy endolysosomal system fusion hypoxia-ischemia brain mitophagy N-ethylmaleimide-sensitive protein TMEM175

Electroacupuncture reduces apoptotic index and inhibits p38 mitogen-activated protein kinase signaling pathway in the hippocampus of rats with cerebral ischemia/reperfusion injury

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Neural Regeneration Research 2017年第3期12卷 409-416页

作者： Xiao Lan Xin Zhang Guo-ping Zhou Chun-xiao Wu Chun Li Xiu-hong Xu School of Traditional Chinese Medicine Southern Medical University College of Acupuncture Moxibustion and TuinaHunan University of Chinese Medicine

Electroacupuncture attenuates cerebral hypoxia and neuronal apoptosis induced by cerebral ischemia/reperfusion *** further identify the involved mechanisms,we assumed that electroacupuncture used to treat cerebral ischemia/reperfusion injury was associated with the p38 mitogen-activated protein kinase（MAPK） signaling *** established rat models of cerebral ischemia/reperfusion injury using the modified Zea-Longa＇s *** 30 minutes before model establishment,p38 MAPK blocker SB20358 was injected into the left lateral *** 1.5 hours after model establishment,electroacupuncture was administered at acupoints of Chize（LU5）,Hegu（LI4）,Zusanli（ST36）,and Sanyinjiao（SP6） for 20 minutes in the affected *** showed that the combination of EA and SB20358 injection significantly decreased neurologic impairment scores,but no significant differences were determined among different interventional ***-eosin staining also showed reduced brain tissue *** with the SB20358 group,the cells were regularly arranged,the structures were complete,and the number of viable neurons was higher in the SB20358 ＋ electroacupuncture *** deoxynucleotidyl transferase（Td T）-mediated d UTP nick-end labeling assay showed a decreased apoptotic index in each group,with a significant decrease in the SB20358 ＋ electroacupuncture *** revealed reduced phosphorylated p38 expression at 3 days in the electroacupuncture group and SB20358 ＋ electroacupuncture group compared with the ischemia/reperfusion *** was no significant difference in phosphorylated p38 expression between the ischemia/reperfusion group and SB20358 *** findings confirmed that the electroacupuncture effects on mitigating cerebral ischemia/reperfusion injury are possibly associated with the p38 MAPK signaling pathway.A time period of 3 days could promote the repair of ischemic cerebral nerves.

关键词： nerve regeneration brain injury electroacupuncture cell apoptosis cerebral ischemia/reperfusion injury neurological impairment score morphological changes immunohistoehemical assay p38 mitogen-activated protein kinases phosphorylated p38 hippocampus neural regeneration

Danhong injection A modulator for Golgi structural stability after cerebral ischemiareperfusion injury

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Neural Regeneration Research 2013年第25期8卷 2343-2349页

作者： Yan Wang Zhiping Hu Wei Lu Department of Neurology Second Xiangya HospitalCentral South University

The cerebral ischemia-reperfusion model was established using the suture occlusion method, and rats were intraperitoneally given 8 mL/kg Danhong injection once a day prior to model establishment Rat brain tissues were harvested at 6, 24, 48, 72 hours after reperfusion. Immunohistochemical staining showed that transforming growth factor-J31 expression increased, while Golgi matrix protein GM130 expression decreased after cerebral ischemia-reperfusion. Danhong injection was shown to significantly up-regulate the expression of transforming growth factor-131 and GM130, and expres- sion levels peaked at 7 days after reperfusion. At 7 days after cerebral ischemia-reperfusion, Golgi morphology was damaged in untreated rats, while Golgi morphology breakage was not observed after intervention with Danhong injection. These experimental findings indicate that Danhong injec- tion can up-regulate the expression of transforming growth factor-131 and GM130, and maintain Golgi stability, thus playing a neuroprotective role in rats after cerebral ischemia-reperfusion.

关键词： neural regeneration traditional Chinese medicine Danhong injection cerebral ischemia-reperfu-sion transforming growth factor-131 GM130 Goigi matrix protein brain injury neuroprotection grants-supported paper neuroregeneration

Tall gastrodis tuber combined with antiepileptic drugs repairs abnormal perfusion foci in focal epilepsy

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Neural Regeneration Research 2013年第3期8卷 208-217页

作者： Weimin Wang Zhenyu Fan Yongqin Zhang Yuxia Yang Yaqing Liu Xiaoli Dang Wenjun Song Yinping Wu Jiang Ye Epilepsy Center Second HospitalLanzhou UniversityGansu Provincial Center for Prevention and Treatment of Epilepsy

One hundred patients with focal epilepsy were recruited for the present study and their seizures controlled with antiepileptic drugs. The patients then orally received a capsule of tall gastrodis tuber powder, a traditional Chinese drug, and underwent single photon emission computed tomography, long-term electroencephalogram, and CT/MRI. Blood drug levels were monitored throughout the study. Before treatment with tall gastrodis tuber, 35 of the 100 cases had abnormal CT/MRI scans; 79 cases had abnormal single photon emission computed tomography images; 86 cases had abnormal electroencephalogram; and a total of 146 abnormal perfusion foci were observed across the 100 subjects. After treatment, the number of patients with normal single photon emission computed tomography images increased by 12; normal electroencephalogram was observed in an additional 27 cases and the number of patients with epileptiform discharge decreased by 29 （34% of 86）; the total number of abnormal perfusion foci decreased by 52 （36%） and changes in abnormal loci were visible in 65 patients. These changes indicate that the administration of tall gastrodis tuber in combination with antiepileptic drugs repairs abnormal perfusion foci in patients with focal epilepsy Our results demonstrate that traditional Chinese drugs can repair abnormal perfusion foci and, as such, are a promising new pathway in the treatment of focal epilepsy.

关键词： neural regeneration traditional Chinese medicine neuroimaging brain injury tall gastrodis tuber antiepileptic drugs combination therapy focal epilepsy abnormal perfusion focus single photonemission computed tomography long-term vigilance-controlled electroencephalogram region ofinterest grant-supported paper photographs-containin^l paper: neuoreaeneration

What is the new target inhibiting the progression of Alzheimer's disease?

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Neural Regeneration Research 2013年第21期8卷 1938-1947页

作者： Lin Zhang Jing Yang Yunpeng Cao Department of Neurology First Affiliated Hospital of China Medical University Provincial Key Laboratory of Cardiovascular and Cerebrovascular Drug Basic Research Liaoning Medical University

To stop the progression of Alzheimer＇s disease in the early stage, it is necessary to identify new therapeutic targets. We examined striatal-enriched phosphatase 61 expression in the brain tissues of 12-month-old APPswe/PSEN1dE9 transgenic mice. Immunohistochemistry showed that striatal-enriched phosphatase 61 protein expression was significantly increased but phosphorylated N-methyl-D-aspartate receptor 2B levels were significantly decreased in the cortex and hippocampus of APPswe/PSEN1dE9 transgenic mice. Western blotting of a cell model of Alzheimer＇s disease consisting of amyloid-beta peptide （1-42）-treated C57BL/6 mouse cortical neurons in vitro showed that valeric acid （AP5）, an N-methyl-D-aspartate receptor antagonist, significantly inhibited amyloidbeta 1-42-induced increased activity of striatal-enriched phosphatase 61. In addition, the phosphorylation of N-methyl-D-aspartate receptor 2B at Tyr1472 was impaired in amyloid-beta 1-42-treated cortical neurons, but knockdown of striatal-enriched phosphatase 61 enhanced the phosphorylation of N-methyl-D-aspartate receptor 2B. Collectively, these findings indicate that striatal-enriched phosphatase 61 can disturb N-methyl-D-aspartate receptor transport and inhibit the progression of learning and study disturbances induced by Alzheimer＇s disease. Thus, striatal-enriched phosphatase 61 may represent a new target for inhibiting the progression of Alzheimer＇s disease.

关键词： neural regeneration brain injury neurodegeneration Alzheimer’s disease striatal-enriched phosphatase 61 amyloid-beta peptide N-methyl-D-aspartate receptor GluN2B RNA interference immunohistochemistry western blot neuroregeneration

miR-137, a new target for post-stroke depression?

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Neural Regeneration Research 2013年第26期8卷 2441-2448页

作者： Lixia Zhao Huazi Li Ruiyou Guo Teng Ma Rongyao Hou Xiaowei Ma Yifeng Du Department of Neurology Shandong Provincial Hospital Department of Neurology Haici Hospital Affiliated to Medical College of Qingdao University Department of Medical Imaging Haici Hospital Affiliated to Medical College of Qingdao University

Expression of miR-137 is downregulated in brain tissue from patients with depression and suicidal behavior, and is also downregulated in peripheral blood from stroke patients. However, it is not yet known if miR-137 acts as a bridge between stroke and depression. To test this, we used middle cerebral artery occlusion and chronic mild stress to establish a post-stroke depression model in rats. Compared with controls, we found significantly lower miR-137 levels in the brain and peripheral blood from post-stroke depression rats. Injection of a miR-137 antagonist into the brain ventricles upregulated miR-137 levels, and improved behavioral changes in post-stroke depression rats. Luciferase assays showed miR-137 bound to the 3＇UTR of Grin2A, regulating Grin2A expression in a neuronal cell line. Grin2A gene overexpression in the brain of post-stroke depression rats, no- ticeably suppressed the inhibitory effect of miR-137 on post-stroke depression. Overall, our results show that miR-137 suppresses Grin2A protein expression through binding to Grin2A mRNA, thereby exerting an inhibitory effect on post-stroke depression. Our results offer a new therapeutic direction for post-stroke depression.

关键词： neural regeneration brain injury post-stroke depression microRNA cerebrovascular disease Grin2A miR-137 neuroregeneration

Neurotransmitter regulation of extracellular signal-regulated kinase expression following subarachnoid hemorrhage

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Neural Regeneration Research 2010年第3期5卷 214-220页

作者： Jinning Song Wenbo Wang Long Sui Department of Neurosurgery First Affiliated Hospital of Medical College Xi'an Jiaotong University Xi'an 710061 Shaanxi Province China

BACKGROUND： Very few studies have addressed neuronal injury in cerebral vasospasm and subarachnoid hemorrhage （SAH）, and the role of neurotransmitters in the regulation of extracellular signal-regulated kinase 1/2 （ERK1/2） expression following SAH. OBJECTIVE： To analyze neurotransmitter regulation of ERK1/2 expression through the use of signal transduction, and to investigate cerebral injury mechanisms following SAH. DESIGN, TIME AND SETTING： A completely randomized grouping and controlled animal experiment was performed at the Experimental Center of Medical College of Xi＇an Jiaotong University from March to December 2008. MATERIALS： Extraceliular signal-regulated ERK1/2 polyclonal antibody and streptavidin-peroxidase method kits were purchased from Beijing Biosynthesis Biotechnology, China; DAB kit was purchased from Zhongshan Golden Bridge Biotechnology, China; TUNEL kit was purchased from Promega, USA. METHODS： A total of 114 male, Sprague Dawley rats, aged 55-63 days old, were randomly assigned to five groups： SAH （n = 30）, saline control （n = 30）, puncture control （n = 30）, normal control （n = 6）, and neurotransmitter-treated （n = 18）. The SAH model was established by twice injecting blood through the cisterna magna. The neurotransmitters-treated group was subdivided into three groups according to drugs injected into the lateral cerebral ventricle： acetylcholine chloride, norepinephrine, and saline, with six animals in each group. MAIN OUTCOME MEASURES： Rats from the SAH, saline control, and puncture control groups were respectively sacrificed at 6, 12, and 24 hours, as well as 3 and 5 days, with six rats at each time point. The normal control group rats were sacrificed at 6 hours, and the neurotransmitter group rats were sacrificed 3 days following neurotransmitter injection. Morphological cellular changes were observed by hematoxylin and eosin staining. Immunohistochemical SP method was used to detect expression of ERK1/2 in the cortex, and cortical apoptosis

关键词： extracellular signal-regulated kinase subarachnoid hemorrhage apoptosis neurotransmitters brain injury neural regeneration

Carbenoxolone pretreatment and treatment of posttraumatic epilepsy

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Neural Regeneration Research 2013年第2期8卷 169-176页

作者： Weiguan Chen Zhiwei Gao Yaohui Ni Zhenxiang Dai Department of Rehabilitation Medicine Affiliated Hospital of Nantong University Department of Neurology Affiliated Hospital of Nantong University

Gap junction blocking agents can inhibit spontaneous discharge frequency in cells. We established a rat model of posttraumatic epilepsy induced using ferric ions. Rats were intraperitoneally injected with carbenoxolone, 20 mg/kg, prior to and 30 minutes after model establishment, once a day for 14 consecutive days. Immunohistochemistry showed glial cell proliferation around a cortical focus and significantly increased connexin expression in posttraumatic epilepsy. However, carbenoxolone pretreatment or treatment significantly reduced connexin expression in the cortex, inhibited glial fibdllary acidic protein expression and ameliorated seizure degree in rats. These findings indicate that large amounts of glial cell proliferation and abnormal gap junction generation play a role in posttraumatic epilepsy, and that carbenoxolone may prevent and treat this disease.

关键词： neural regeneration brain injury posttraumatic epilepsy ferric ion gap junction carbenoxolone glial fibrillary acidic protein connexin 43 seizure brain injury grant-supported paper photographs-containing paper neuroregeneration

Mild hypothermia combined with neural stem cell transplantation for hypoxic-ischemic encephalopathy: neuroprotective effects of combined therapy

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Neural Regeneration Research 2014年第19期9卷 1745-1752页

作者： Lin Wang Feng Jiang Qifeng Li Xiaoguang He Jie Ma Department of Pediatric Neurosurgery Xinhua Hospital of Shanghai Jiaotong University

Neural stem cell transplantation is a useful treatment for ischemic stroke, but apoptosis often occurs in the hypoxic-ischemic environment of the brain after cell transplantation. In this study, we determined if mild hypothermia （27-28~C） can increase the survival rate of neural stem cells （1.0 x 105/~tL） transplanted into neonatal mice with hypoxic-ischemic encephalopathy. Long-term effects on neurological functioning of the mice were also examined. After mild hy- pothermia combined with neural stem cell transplantation, we observed decreased expression levels of inflammatory factor nuclear factor-kappa B and apoptotic factor caspase-3, reduced cerebral infarct volumes, increased survival rate of transplanted cells, and marked improvements in neurological function. Thus, the neuroprotective effects of mild hypothermia combined with neural stem cell transplantation are superior to those of monotherapy. Moreover, our findings suggest that the neuroprotective effects of mild hypothermia combined with neural stem cell transplantation on hypoxic-ischemic encephalopathy are achieved by anti-inflammatory and an- ti-apoptotic mechanisms.

关键词： nerve regeneration brain injury hypoxic-ischemic encephalopathy neural precursorcells hypothermia neural stem cells cell transplantation hippocampus neuron cell apoptosis astrocytes oligodendrotytes neuroprotection NSFC grants neural regeneration