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The action mechanism by which C1q/tumor necrosis factor-related protein-6 alleviates cerebral ischemia/reperfusion injury in diabetic mice

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Neural Regeneration Research 2024年第9期19卷 2019-2026页

作者： Bo Zhao Mei Li Bingyu Li Yanan Li Qianni Shen Jiabao Hou Yang Wu Lijuan Gu Wenwei Gao Department of Anesthesiology Renmin Hospital of Wuhan UniversityWuhanHubei ProvinceChina Central Laboratory Renmin Hospital of Wuhan UniversityWuhanHubei ProvinceChina Department of Critical Care Medicine Renmin Hospital of Wuhan UniversityWuhanHubei ProvinceChina

Studies have shown that C1q/tumor necrosis factor-related protein-6 (CTRP6) can alleviate renal ischemia/reperfusion injury in mice. However, its role in the brain remains poorly understood. To investigate the role of CTRP6 in cerebral ischemia/reperfusion injury associated with diabetes mellitus, a diabetes mellitus mouse model of cerebral ischemia/reperfusion injury was established by occlusion of the middle cerebral artery. To overexpress CTRP6 in the brain, an adeno-associated virus carrying CTRP6 was injected into the lateral ventricle. The result was that oxygen injury and inflammation in brain tissue were clearly attenuated, and the number of neurons was greatly reduced. In vitro experiments showed that CTRP6 knockout exacerbated oxidative damage, inflammatory reaction, and apoptosis in cerebral cortical neurons in high glucose hypoxia-simulated diabetic cerebral ischemia/reperfusion injury. CTRP6 overexpression enhanced the sirtuin-1 signaling pathway in diabetic brains after ischemia/reperfusion injury. To investigate the mechanism underlying these effects, we examined mice with depletion of brain tissue-specific sirtuin-1. CTRP6-like protection was achieved by activating the sirtuin-1 signaling pathway. Taken together, these results indicate that CTRP6 likely attenuates cerebral ischemia/reperfusion injury through activation of the sirtuin-1 signaling pathway.

关键词： brain C1q/tumor necrosis factor-related protein-6 cerebral apoptosis diabetes inflammation ischemia/reperfusion injury neuron neuroprotection oxidative damage Sirt1

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Homer1a reduces inflammatory response after retinal ischemia/reperfusion injury

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Neural Regeneration Research 2024年第7期19卷 1608-1617页

作者： Yanan Dou Xiaowei Fei Xin He Yu Huan Jialiang Wei Xiuquan Wu Weihao Lyu Zhou Fei Xia Li Fei Fei Department of Neurosurgery Xijing HospitalAir Force Military Medical UniversityXi’anShaanxi ProvinceChina Department of Ophthalmology Xijing HospitalAir Force Military Medical UniversityXi’anShaanxi ProvinceChina

Elevated intraocular pressure(IOP)is one of the causes of retinal ischemia/reperfusion injury,which results in NRP3 inflammasome activation and leads to visual *** is repo rted to play a protective role in neuroinflammation in the ***,the effects of Homerla on NLRP3inflammasomes in retinal ischemia/reperfusion injury caused by elevated IOP remain *** our study,animal models we re constructed using C57BL/6J and Homer1^(flox/-)/Homerla^(+/-)/Nestin-Cre^(+/-)mice with elevated IOP-induced retinal ischemia/repe rfusion *** in vitro expe riments,the oxygen-glucose deprivation/repe rfusion injury model was constructed with M uller *** found that Homerla ove rexpression amelio rated the decreases in retinal thickness and Muller cell viability after ischemia/reperfusion ***,Homerla knockdown promoted NF-κB P65^(Ser536)activation via caspase-8,NF-κB P65 nuclear translocation,NLRP3 inflammasome formation,and the production and processing of interleukin-1βand inte *** opposite results we re observed with Homerla ove ***,the combined administration of Homerla protein and JSH-23 significantly inhibited the reduction in retinal thickness in Homer1^(flox/-)Homer1a^(+/-)/Nestin-Cre^(+/-)mice and apoptosis in M uller cells after ischemia/reperfusion *** together,these studies demonstrate that Homer1a exerts protective effects on retinal tissue and M uller cells via the caspase-8/NF-KB P65/NLRP3 pathway after I/R injury.

关键词： caspase-8 Homer1a interleukin-18 interleukin-1β intraocular pressure ischemia/reperfusion injury JSH-23 Müller cells NLRP3 nuclear factor-kB p65 retina

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C-reactive protein aggravates myocardial ischemia/reperfusion injury through activation of extracellular-signal-regulated kinase 1/2

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Journal of Geriatric Cardiology 2018年第7期15卷 502-513页

作者： Wei-Na PEI Hai-Juan HU Fan LIU Bing XIAO Ya-Bei ZUO Wei CUI Department of Cardiology Second Hospital of Hebei Medical University and Institute of Cardiocerebrovascular Disease of Hebei Province Shijiazhuang Hebei China

Background ischemia/reperfusion injury （IRI） is an inflammatory response that occurs when tissue is reperfused following a prolonged period of ischemia. Several studies have indicated that C-reactive protein （CRP） might play an important role in inducing IRI. However, the effects of CRP on myocardial IRI and the underlying mechanisms have not been fully elucidated. This study aimed to investigate the association between CRP and myocardial IRI and the underlying mechanisms. Methods We simulated ischemia/reperfusion using oxygen-glucose deprivation/ reoxygenation （OGD/R） in neonatal Sprague-Dawley rat cardiomyocytes; reperfusion injury was induced by three hours of hypoxia with glucose and serum deprivation followed by one hour of reperfusion. Cell viability was tested with MTS assays, and cardiomyocyte damage was evaluated by lactate dehydrogenase （LDH） leakage. Mitochondrial membrane potential was measured using tetramethylrhodamine ethyl ester （TMRE） and mitochondrial permeability transition pore （mPTP） opening was measured using calcein/AM; both TMRE and caocein/AM were visualized with laser scanning confocal microscopy. In addition, we studied the signaling pathways underlying CRP-mediated ischemia/reperfusion injury via Western blot analysis. Results Compared with the simple OGD/R group, after intervention with 10 pg/mL CRP, cell viability decreased markedly （82.36 % ± 6.18% vs. 64.84% ± 4.06%, P = 0.0007）, and the LDH leakage significantly increased （145.3 U/L ± 16.06 U/L vs. 208.2 U/L ± 19.23 U/L, P = 0.0122）. CRP also activated mPTP opening and reduced mitochondrial membrane potential during myocardial ischemia/reperfusion. Pretreatment with 1 pM atorvastatin （Ator） before CRP intervention protected cardiomyocytes from IRI. Mitochondrial KATP channel opener diazoxide and mPTP inhibitor cyclosporin A also offset the effects of CRP in this process. The level of phosphorylated extracellular-signal-regulated kinase （ERK） 1/2 was significantly higher after pre-tre

关键词： C-reactive protein ischemia/reperfusion injury Mitochondrial permeability transition pore Mitochondrial KATP channel Statin

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Protective effect of oxysophoridine on cerebral ischemia/reperfusion injury in mice

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Neural Regeneration Research 2013年第15期8卷 1349-1359页

作者： Hongbo Wang Yuxiang Li Ning Jiang Xiaoping Chen Yi Zhang Kuai Zhang Tengfei Wang Yinju Hao Lin Ma Chengjun Zhao Yanrong Wang Tao Sun Jianqiang Yu Department of Pharmacology Ningxia Medical University College of Nursing Ningxia Medical University Shanghai Pudong New Area Gongli Hospital Ningxia Key Laboratory of Craniocerebral Diseases of Ningxia Hui Autonomous Region School of Basic Medical Sciences Ningxia Medical University Key Laboratory of Reproduction and Genetics of Ningxia Medical University Collaborative Innovation Center of Ningxia Hui Autonomous Region for Medicines

Oxysophoridine, a new alkaloid extracted from Sophora alopecuroides L., has been shown to have a protective effect against ischemic brain damage. In this study, a focal cerebral ischemia/reperfusion injury model was established using middle cerebral artery occlusion in mice. Both 62.5, 125, and 250 mg/kg oxysophoridine, via intraperitoneal injection, and 6 mg/kg nimodipine, via intragastric administration, were administered daily for 7 days before modeling. After 24 hours of reperfusion, mice were tested for neurological deficit, cerebral infarct size was assessed and brain tissue was collected. Results showed that oxysophoridine at 125, 250 mg/kg and 6 mg/kg nimodipine could reduce neurological deficit scores, cerebral infarct size and brain water content in mice. These results provided evidence that oxysophoridine plays a protective role in cerebral ischemia/reperfusion injury. In addition, oxysophoridine at 62.5, 125, and 250 mg/kg and 6 mg/kg nimodipine increased adenosine-triphosphate content, and decreased malondialdehyde and nitric oxide content. These compounds enhanced the activities of glutathione-peroxidase, superoxide dismutase, catalase, and lactate dehydrogenase, and decreased the activity of nitric oxide synthase Protein and mRNA expression levels of N-methyI-D-aspartate receptor subunit NR1 were markedly inhibited in the presence of 250 mg/kg oxysophoridine and 6 mg/kg nimodipine. Our experimental findings indicated that oxysophoridine has a neuroprotective effect against cerebral ischemia/reperfusion injury in mice, and that the effect may be due to its ability to inhibit oxidative stress and expression of the N-methyI-D-aspartate receptor subunit NR1.

关键词： neural regeneration traditional Chinese medicine brain injury oxysophoridine ischemia/reperfusion injury oxidative stress N-methyI-D-aspartate receptor neuroprotection grants-supported paper neuroregeneration

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Effects of kallikrein gene transfer on penumbral microvascular proliferation and on regional cerebral blood flow following cerebral ischemia/reperfusion injury

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Neural Regeneration Research 2008年第10期3卷 1045-1050页

作者： Ruiyan Lu Qingyu Shen Lianhong Yang Mei Li Yidong Wang Ying Peng Department of Neurology Second Affiliated Hospital of Sun Yat-sen University Guangzhou 510120 Guangdong Province China

BACKGROUND： Recent findings have demonstrated that the kallikrein-kinin system （KKS） participates in the pathological process of cerebral ischemia/reperfusion injury. Kallikrein gene transfer exhibits neural protective effects following cerebral infarction. OBJECTIVE： To observe the effects of kallikrein gene transfer on vascular proliferation in the peripheral infarct focus and on regional cerebral blood flow （rCBF） following cerebral ischemia/reperfusion injury. DESIGN, TIME AND SETTING： The completely randomized, controlled experiment was performed at the Lin Baixin Laboratory Center, the Second Affiliated Hospital of Sun Yat-sun University between September 2007 and April 2008. MATERIALS： pUCI9-HTK plasmid was constructed and maintained in the Laboratory for Neurology, the Second Affiliated Hospital of Sun Yat-sen University, China. Mouse anti-human kallikrein 1 monoclonal antibody was purchased from R＆D Systems, USA. METHODS Ninety healthy, male, Sprague Dawley rats were used. Middle cerebral artery occlusion （MCAO） was established in all rats to induce cerebral ischemia/reperfusion injury. Following MCAO establishment, all rats were randomly divided into three groups （n = 30）： blank control, saline, and pAdCMV-HTK. The saline and pAdCMV-HTK groups were stereotactically micro-injected with 5μL of physiological saline or with pAdCMV-HTK [multiplicity of infection （MOI） = 20], respectively, into the ischemic penumbra. In the blank control group, only sham injection was performed. MAIN OUTCOME MEASURES： At 12, 24, and 72 hours after treatment, cerebral infarction volume was measured by 2, 3, 5-triphenyltetrazolium chloride （TTC） staining. Exogenous HTK expression, as well as regional vascular endothelial growth factor （VEGF） expression, was detected by immunohistochemistry. rCBF was examined by 14C-iodoantipyrine micro tracing. In addition, neurological severity score （NSS） was performed. Higher scores indicated more severe neurological deficits. RESULTS： NSS resu

关键词： cerebral ischemia ischemia/reperfusion injury adenovirus gene transfer kallikrein vascular endothelial growth factor perfusion, regional

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Ginsenoside Rd inhibits apoptosis following spinal cord ischemia/reperfusion injury

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Neural Regeneration Research 2014年第18期9卷 1678-1687页

作者： Baogang Wang Qingsan Zhu Xiaxia Man Li Guo Liming Hao Department of Cardiac Surgery First Hospital of Jilin University Department of Orthopedics China-Japan Union Hospital of Jilin University Department of Oncological Gynecology First Hospital of Jilin University Department of Toxicology School of Public HealthJilin University Department of Histology and Embryology College of Basic Medical SciencesJilin University

Ginsenoside Rd has a clear neuroprotective effect against ischemic stroke. We aimed to verify the neuroprotective effect of ginsenoside Rd in spinal cord ischemia/reperfusion injury and explore its anti-apoptotic mechanisms. We established a spinal cord ischemia/reperfusion injury model in rats through the occlusion of the abdominal aorta below the level of the renal artery for 1 hour. Successfully established models were injected intraperitoneally with 6.25, 12.5, 25 or 50 mg/kg per day ginsenoside Rd. Spinal cord morphology was observed at 1, 3, 5 and 7 days after spinal cord ischemia/reperfusion injury. Intraperitoneal injection of ginsenoside Rd in ischemia/reperfusion injury rats not only improved hindlimb motor function and the morphology of motor neurons in the anterior horn of the spinal cord, but it also reduced neuronal apoptosis. The optimal dose of ginsenoside Rd was 25 mg/kg per day and the optimal time point was 5 days after ischemia/ reperfusion. Immunohistochemistry and western blot analysis showed ginsenoside Rd dose-de- pendently inhibited expression of pro-apoptotic Caspase 3 and down-regulated the expression of the apoptotic proteins ASK1 and JNK in the spinal cord of rats with spinal cord ischemia/reper- fusion injury. These findings indicate that ginsenoside Rd exerts neuroprotective effects against spinal cord ischemia/reperfusion injury and the underlying mechanisms are achieved through the inhibition of ASK1-JNK pathway and the down-regulation of Caspase 3 expression.

关键词： nerve regeneration spinal cord injury ginsenoside Rd ischemia/reperfusion injury apoptosis ASKI INK Caspase 3 neural regeneration

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Argon reduces microglial activation and inflammatory cytokine expression in retinal ischemia/reperfusion injury

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Neural Regeneration Research 2021年第1期16卷 192-198页

作者： Ulrich Goebel Stefanie Scheid Sashko Spassov Nils Schallner Jakob Wollborn Hartmut Buerkle Felix Ulbrich Department of Anesthesiology and Critical Care Medical Center–University of FreiburgFaculty of MedicineUniversity of FreiburgFreiburgGermany

We previously found that argon exerts its neuroprotective effect in part by inhibition of the toll-like receptors(TLR)2 and *** downstream transcription factors signal transducer and activator of transcription 3(STAT3)and nuclear factor kappa B(NF-κB)are also affected by argon and may play a role in *** also has been demonstrated that argon treatment could mitigate brain damage,reduce excessive microglial activation,and subsequently attenuate brain *** intensive research,the further exact mechanism remains *** this study,human neuroblastoma cells were damaged in vitro with rotenone over a period of 4 hours(to mimic cerebral ischemia and reperfusion damage),followed by a 2-hour post-conditioning with argon(75%).In a separate in vivo experiment,retinal ischemia/reperfusion injury was induced in rats by increasing intraocular pressure for 1 *** reperfusion,argon was administered by inhalation for 2 *** reduced the binding of the transcription factors signal transducer and activator of transcription 3,nuclear factor kappa B,activator protein 1,and nuclear factor erythroid 2-related factor 2,which are involved in regulation of neuronal *** cytometry analysis showed that argon downregulated the Fas *** transcription factors were regulated by toll-like receptors;therefore,their effects could be eliminated,at least in part,by the TLR2 and TLR4 inhibitor oxidized phospholipid 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine(OxPAPC).Argon treatment reduced microglial activation after retinal ischemia/reperfusion *** quantitative polymerase chain reaction analysis revealed a reduction in the pro-inflammatory cytokines interleukin(IL-1α),IL-1β,IL-6,tumor necrosis factorα,and inducible nitric oxide *** results suggest that argon reduced the extent of inflammation in retinal neurons after ischemia/reperfusion injury by suppression of transcription factors crucial for microglial

关键词： argon ischemia/reperfusion injury microglia neuroinflammation neuroprotection noble gas SH-SY5Y toll-like receptor transcription factor

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An optimal dose of tea polyphenols protects against global cerebral ischemia/reperfusion injury

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Neural Regeneration Research 2013年第9期8卷 783-791页

作者： Jianrui Lv Rongliang Xue Jing Zhao Xin Wei Hui Gao Rongguo Fu Gang Wu Wei Li Xiaoming Lei Junbin Tian Department of Anesthesiology Second Affiliated Hospital Medical School of Xi'an Jiaotong University

Previous studies addressing the protection of tea polyphenols against cerebral ischemia/ reperfusion injury often use focal cerebral ischemia models, and the optimal dose is not unified. In this experiment, a cerebral ischemia/reperfusion injury rat model was established using a modified four-vessel occlusion method. Rats were treated with different doses of tea polyphenols （25, 50, 100, 150, 200 mg/kg） via intraperitoneal injection. Results showed that after 2, 6, 12, 24, 48 and 72 hours of reperfusion, peroxide dismutase activity and total antioxidant capacity in brain tissue gradually increased, while malondialdehyde content gradually decreased after tea polyphenol intervention. Tea polyphenols at 200 mg/kg resulted in the most apparent changes. Terminal deoxynucleotidyl transferase-mediated nick end labeling and flow cytometry showed that 200 mg/kg tea polyphenols significantly reduced the number and percentage of apoptotJc cells in the hippocampal CA1 region of rats after cerebral ischemia/reperfusion injury. The open field test and elevated plus maze experiments showed that tea polyphenols at 200 mg/kg strengthened exploratory behavior and reduced anxiety of cerebral ischemia/reperfusion injured rats. Experimental findings indicate that tea polyphenols protected rats against cerebral ischemia/ reperfusion injury and 200 mg/kg is regarded as the optimal dose.

关键词： neural regeneration brain injury traditional Chinese medicine tea polyphenols brain ischemia/reperfusion injury oxidative stress neuroethology apoptosis grants-supported paper photographs-containing paper neuroregeneration

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The mechanisms through which auricular vagus nerve stimulation protects against cerebral ischemia/reperfusion injury

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Neural Regeneration Research 2022年第3期17卷 594-600页

作者： Jing-Jun Zhao Zheng-Hui Wang Ying-Jie Zhang Wen-Jing Wang Ai-Fang Cheng Pei-Jing Rong Chun-Lei Shan Center of Rehabilitation Medicine Yueyang Hospital of Integrated Traditional Chinese and Western MedicineShanghai University of Traditional Chinese MedicineShanghaiChina School of Rehabilitation Science Shanghai University of Traditional Chinese MedicineShanghaiChina Engineering Research Center of Traditional Chinese Medicine Intelligent Rehabilitation Ministry of EducationShanghaiChina Center of Rehabilitation Medicine the First Affiliated Hospital of Xinxiang Medical UniversityXinxiangHenan ProvinceChina Shanghai Research Institute of Acupuncture and Meridian ShanghaiChina Institute of Acupuncture and Moxibustion Chinese Academy of Chinese Medical SciencesBeijingChina

Previous studies have shown that vagus nerve stimulation can improve patients' locomotor *** stimulation of the auricular vagus nerve,which is the only superficial branch of the vagus nerve,may have similar effects to vagus nerve ***,the precise mechanisms remain poorly *** this study,rat models of cerebral ischemia/reperfusion injury were established by modified Longa ***-four hours later,7-day auricular vagus nerve stimulation was *** results showed that auricular vagus nerve stimulation promoted the secretion of acetylcholine,inhibited the secretion of interleukin-1β,interleukin-6,and tumor necrosis factor-α,and reduced connexin 43 phosphorylation in the ischemic penumbra and motor cortex,promoting locomotor function recovery in rats with cerebral ischemia/reperfusion *** findings suggested that auricular vagus nerve stimulation promotes the recovery of locomotor function in rats with cerebral ischemia/reperfusion injury by altering the secretion of acetylcholine and inflammatory factors and the phosphorylation of connexin *** study was approved by the Animal Use and Management Committee of Shanghai University of Traditional Chinese Medicine on November 8,2019(approval ***191108014).

关键词： auricular vagus nerve stimulation connexin 43 gap junction inflammatory factor ischemia/reperfusion injury neurological function neuroprotection stroke

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High-throughput sequencing analysis of differentially expressed mi RNAs and target genes in ischemia/reperfusion injury and apelin-13 neuroprotection

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Neural Regeneration Research 2018年第2期13卷 265-271页

作者： Chun-mei Wang Xue-lu Yang Ming-hui Liu Bao-hua Cheng Jing Chen Bo Bai Neurobiology Institute Jining Medical University

miRNAs regulate a variety of biological processes through pairing-based regulation of gene expression at the 3＇ end of the noncoding region of the target miRNA, miRNAs were found to be abnormally expressed in ischemia/reperfusion injury models. High-throughput sequencing is a recently developed method for sequencing miRNAs and has been widely used in the analysis of miRNAs. In this study, ischemia/reperfusion injury models were intracerebroventricularly injected with 50 pg/kg apelin-13. High-throughput sequencing showed that 357 known miRNAs were differentially expressed among rat models, among which 78 changed to 〉 2-fold or 〈 0.5-fold. Quantita- tive real-time polymerase chain reaction was selected to confirm the expression levels of four miRNAs that were differentially expressed, the results of which were consistent with the results of high-throughput sequencing. Gene Ontology analysis revealed that the predicted targets of the different miRNAs are particularly associated with cellular process, metabolic process, single-organism process, cell, and binding. Kyoto Encyclopedia of Gene and Genome analysis showed that the target genes are involved in metabolic pathways, mitogen-ac- tivated protein kinase signaling pathway, calcium signaling pathway, and nuclear factor-KB signaling pathway. Our findings suggest that differentially expressed miRNAs and their target genes play an important role in ischemia/reperfusion injury and neuroprotection by apelin-13.

关键词： nerve regeneration RNA sequencing microRNA apelin ischemia/reperfusion injury neuroprotection neuropeptide high-throughput sequencing neural regeneration

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