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

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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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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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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Neuronal effects of SP600125 pretreatment in a rat model of cerebral ischemia/reperfusion injury Inhibited down-regulation of DNA repair protein

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Neural Regeneration Research 2009年第12期4卷 1055-1061页

作者： Ning Wang Rongliang Xue Fengzhen Yao Jiaxuan He Jianrui Lu Pengbo Zhang Gang Wu Department of Anesthesiology Second Affiliated Hospital Xi'an Jiaotong University Xi'an 710004 Shaanxi province China Department of Anesthesiology Jiangsu Province Hospital of Traditional Chinese Medicine Nanjing 210002 Jiangsu province China

BACKGROUND： Recent studies have shown that the selective inhibitor of c-Jun N-terminal kinases （JNKs） signaling pathway, SP600125, exhibits neuronal protective effects in a rat model of brain ischemia/reperfusion. OBJECTIVE： To determine the mechanisms of neuroprotective effects of SP600125 in a rat model of brain ischemia/reperfusion, and determine the role of the JNK signaling pathway in SP600125-induced effects. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Animal Experiment Center, Medical School of Xi＇an Jiaotong University from June 2007 to September 2008. MATERIALS： SP600125 was provided by Biosource, USA; rabbit anti-phospho-JNK （Thr183/Tyr185） polyclonal antibody from Cell Signaling Technology, USA; rabbit anti-X-ray repair cross-complementing protein 1 （XRCC1） and anti-Ku70 polyclonal antibodies from Santa Cruz Biotechnology, USA; and TUNEL kit from Beijing Huamei Biology, China. METHODS： A total of 108 male, 4-month-old, Sprague Dawley rats were randomly assigned to three groups, with 36 rats per group. The sham operation group and ischemia/reperfusion group （I/R group） were intracerebroventricularly injected with 10 μL 1% DMSO. The SP600125-treated group （pre-SP group） was given 10 μL SP600125 （3 μg/μL）. Thirty minutes later, brain ischemia was induced in the I/R and pre-SP groups using the four-vessel occlusion method. Specifically, whole brain ischemia was induced for 6 minutes, and the clips were released to restore carotid artery blood flow. Rats from each group were observed at 2, 6, 12, 24, 48, and 72 hours, with 6 rats for each time point. The sham operation group was treated with the same surgical exposure procedures, with exception of occlusion of the carotid artery. MAIN OUTCOME MEASURES： Hematoxylin-eosin staining was used to observe neuronal survival in the hippocampal CA1 region, TUNEL was used to detect apoptosis in the hippocampal CA1 region, and immunohistochemistry was used to detect expressio

关键词： ischemia/reperfusion injury apoptosis c-Jun N-terminal kinases DNA repair protein X-ray repair cross-complementing protein 1 Ku70

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Propofol regulates Ca～(2+),Mg～(2+),Cu～(2+) and Zn～(2+) balance in the spinal cord after ischemia/reperfusion injury

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Neural Regeneration Research 2011年第23期6卷 1786-1790页

作者： Shuzhou Yin Qijing Yu Ji Hu Jie Yang Juan Chen Department of Anesthesiology Suzhou Kowloon Hospital Shanghai Jiao Tong University School of Medicine Suzhou 215021 Jiangsu Province China Department of Anesthesiology Renmin Hospital of Wuhan University Wuhan 430060 Hubei Province China Department of Anesthesiology Liyuan Hospital of Tongji Medical College Huazhong University of Science ＆ Technology Wuhan 430077 Hubei Province China

This study assessed concentrations of Ca2＋, Mg2＋, Cu2＋ and Zn2＋ in blood serum and spinal cord tissues, as well as the possible mechanisms by which propofol may protect spinal cord tissues during ischemia/reperfusion injury. With prolonged duration of ischemia/reperfusion injury, serum Ca2＋ and Cu2＋ concentrations gradually increased, but Mg 2＋ and Zn2＋ concentrations gradually decreased. Seven days after spinal cord injury, changes in Ca2＋, Mg2＋, Cu2＋ and Zn2＋ concentrations were significant. After 7 days of reperfusion, changes in the concentrations of Ca2＋, Mg2＋, Cu2＋ and Zn2＋ in spinal cord homogenates were consistent with those in the serum. After propofol treatment, no significant changes in Ca2＋, Mg2＋, Cu2~ and Zn2＋ concentrations in serum and spinal cord homogenates were noted during ischemia/reperfusion injury. These findings suggest that propofol exerts protective effects against spinal cord injury by stabilizing or recovering metal ion balance in ischemic regions.

关键词： ischemia/reperfusion injury spinal cord propofol Ca2+ Mg2+ Cu2+ Zn2+ neuroprotection.

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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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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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Activated PKB/GSK-3β synergizes with PKC-δ signaling in attenuating myocardial ischemia/reperfusion injury via potentiation of NRF2 activity: Therapeutic efficacy of dihydrotanshinone-Ⅰ

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Acta Pharmaceutica Sinica B 2021年第1期11卷 71-88页

作者： Hao Zengy Lingling Wangy Jiawei Zhang Ting Pan Yinghua Yu Jingxia Lu Ping Zhou Hua Yang Ping Li State Key Laboratory of Natural Medicines School of Traditional Chinese PharmacyChina Pharmaceutical UniversityNanjing 210009China

Disrupted redox status primarily contributes to myocardial ischemia/reperfusion injury(MIRI).NRF2,the endogenous antioxidant regulator,might provide therapeutic ***-Ⅰ(DT)is an active component in Salvia miltiorrhiza with NRF2 induction *** study seeks to validate functional links between NRF2 and cardioprotection of DT and to investigate the molecular mechanism particularly emphasizing on NRF2 cytoplasmic/nuclear *** potently induced NRF2 nuclear accumulation,ameliorating post-reperfusion injuries via redox *** cardioprotection in NRF2-deficient mice and cardiomyocytes strongly supports NRF2-dependent cardioprotection of ***,DT phosphorylated NRF2 at Ser40,rendering its nuclear-import by dissociating from KEAP1 and inhibiting ***,we identified PKC-δ-(Thr505)phosphorylation as primary upstream event triggering NRF2-(Ser40)*** of PKC-δdramatically retained NRF2 in cytoplasm,convincing its pivotal role in mediating NRF2 ***2 activity was further enhanced by activated PKB/GSK-3βsignaling via nuclear-export signal blockage independent of PKC-δ*** demonstrating independent modulation of PKC-δand PKB/GSK-3β/Fyn signaling,we highlight the ability of DT to exploit both nuclear import and export regulation of NRF2 in treating reperfusion injury harboring redox homeostasis *** of PKC and PKB phenocopied cardioprotection of DT in vitro and in vivo,further supporting the potential applicability of this rationale.

关键词： DihydrotanshinoneⅠ NRF2 Cytoplasmic/nuclear translocation PKC-δ PKB/GSK-3β/Fyn Phosphorylation Redox homeostasis ischemia/reperfusion injury

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Heme oxygenase-1 protects donor livers from ischemia/reperfusion injury:The role of Kupffer cells

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World Journal of Gastroenterology 2010年第10期16卷 1285-1292页

作者： Zeng, Zhong Huang, Han-Fei Chen, Ming-Qing Song, Fei Zhang, Yu-Jun Kunming Med Coll Organ Transplantat Ctr Affiliated Hosp 1 Kunming 650032 Yunnan Province Peoples R China Third Mil Med Univ Southwest Hosp Inst Hepatobiliary Surg Chongqing 400038 Peoples R China

AIM:To examine whether heme oxygenase (HO)-1 overexpression would exert direct or indirect effects on Kupffer cells activation, which lead to aggravation of reperfusion ***: Donors were pretreated with cobalt protoporphyrin (CoPP) or zinc protoporphyrin (ZnPP), HO-1 inducer and antagonist, respectively. Livers were stored at 4℃ for 24 h before transplantation. Kupffer cells were isolated and cultured for 6 h after liver ***: Postoperatively, serum transaminases were significantly lower and associated with less liver injury when donors were pretreated with CoPP, as compared with the ZnPP group. Production of the cytokines tumor necrosis factor-α and interleukin-6 generated by Kupffer cells decreased in the CoPP group. The CD14 expression levels (RT-PCR/Western blots) of Kupffer cells from CoPP-pretreated liver grafts ***: The study suggests that the potential utility of HO-1 overexpression in preventing ischemia/reperfusion injury results from inhibition of Kupffer cells activation.

关键词： Heme oxygenase-1 Kupffer cells ischemia/reperfusion injury Liver transplantation

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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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