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Schisandrin B Inhibits NLRP3 Inflammasome Pathway and Attenuates Early Brain Injury in Rats of Subarachnoid Hemorrhage

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Chinese Journal of Integrative Medicine 2022年第7期28卷 594-602页

作者： CHEN Song DING Yi-hang SHI Song-sheng TU Xian-kun department of neurosurgery Fujian Medical University Union HospitalNeurosurgery Research Institute of Fujian ProvinceFuzhou 350001China

Objective: To determine whether Schisandrin B(Sch B) attenuates early brain injury(EBI) in rats with subarachnoid hemorrhage(SAH). Methods: Sprague-Dawley rats were divided into sham(sham operation), SAH, SAH+vehicle, and SAH+Sch B groups using a random number table. Rats underwent SAH by endovascular perforation and received Sch B(100 mg/kg) or normal saline after 2 and 12 h of SAH. SAH grading, neurological scores, brain water content, Evan’s blue extravasation, and terminal transferase-mediated dUTP nick end-labeling(TUNEL) staining were carried out 24 h after SAH. Immunofluorescent staining was performed to detect the expressions of ionized calcium binding adapter molecule 1(Iba-1) and myeloperoxidase(MPO) in the rat brain, while the expressions of B-cell lymphoma 2(Bcl-2), Bax, Caspase-3, nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3(NLRP3), apoptosis-associated specklike protein containing the caspase-1 activator domain(ASC), Caspase-1, interleukin(IL)-1β, and IL-18 in the rat brains were detected by Western blot. Results: Compared with the SAH group, Sch B significantly improved the neurological function, reduced brain water content, Evan’s blue content, and apoptotic cells number in the brain of rats(P<0.05 or P<0.01). Moreover, Sch B decreased SAH-induced expressions of Iba-1 and MPO(P<0.01). SAH caused the elevated expressions of Bax, Caspase-3, NLRP3, ASC, Caspase-1, IL-1β, and IL-18 in the rat brain(P<0.01), all of which were inhibited by Sch B(P<0.01). In addition, Sch B increased the Bcl-2 expression(P<0.01). Conclusion: Sch B attenuated SAH-induced EBI, which might be associated with the inhibition of neuroinflammation, neuronal apoptosis, and the NLRP3 inflammatory signaling pathway.

关键词： schisandrin B subarachnoid hemorrhage early brain injury inflammation neuronal apoptosis nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 Chinese medicine

Alterations of natural killer cells in traumatic brain injury

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Neuroscience Bulletin 2014年第6期30卷 903-912页

作者： Xiao-Dong Kong Sheng Bai Xin Chen Hui-Jie Wei Wei-Na Jin Min-Shu Li Yaping Yan Fu-Dong Shi departments of Neurology and neurosurgery Key Laboratory of Post-trauma Neuro-repair and Regeneration in the Central Nervous SystemMinistry of EducationTianjin Neurological InstituteTianjin Medical University General Hospital department of Geriatrics Tianjin Geriatrics InstituteTianjin Medical University General Hospital department of Neurology Barrow Neurological InstituteSt.Joseph's Hospital and Medical CenterPhoenixAZUSA

To investigate the relationship between natural killer（NK） cells and traumatic brain injury（TBI）, we tracked an established phenotype of circulating NK cells at several time points in patients with different grades of TBI. In serial peripheral blood samples, NK cells were prospectively measured by flow cytometry of CD3-CD56＋ lymphocytes. Compared to healthy controls, TBI patients had reductions in both the percentage and the absolute number of NK cells. Furthermore, the magnitude of NK cell reduction correlated with the degree of TBI severity at several time points. That is, NK cell population size was independently associated with lower Glasgow Coma Scale scores. In addition, at some time points, a positive correlation was found between the NK cell counts and Glasgow Outcome Scale scores. Our results indicate that TBI induces a reduction in the number of NK cells, and the magnitude of the reduction appears to parallel the severity of TBI.

关键词： natural killer cells traumatic brain injury central nervous system immunity

Dexmedetomidine attenuates traumatic brain injury: action pathway and mechanisms

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Neural Regeneration Research 2018年第5期13卷 819-826页

作者： Dong Wang Xin Xu Yin-Gang Wu Li Lyu Zi-Wei Zhou Jian-Ning Zhang department of neurosurgery Tianjin Medical University General Hospital Tianjin neurological institute Key Laboratory of Post-Neuroinjury Neuro-repair and Regeneration in Central Nervous System Ministry of Education and Tianjin City department of Cardiovascular Tianjin Children's Hospital

Traumatic brain injury induces potent inflammatory responses that can exacerbate secondary blood-brain barrier（BBB） disruption, neuronal injury, and neurological dysfunction. Dexmedetomidine is a novel α2-adrenergic receptor agonist that exert protective effects in various central nervous system diseases. The present study was designed to investigate the neuroprotective action of dexmedetomidine in a mouse traumatic brain injury model, and to explore the possible mechanisms. Adult male C57 BL/6 J mice were subjected to controlled cortical impact. After injury, animals received 3 days of consecutive dexmedetomidine therapy（25 μg/kg per day）. The modified neurological severity score was used to assess neurological deficits. The rotarod test was used to evaluate accurate motor coordination and balance. Immunofluorescence was used to determine expression of ionized calcium binding adapter molecule-1, myeloperoxidase, and zonula occluden-1 at the injury site. An enzyme linked immunosorbent assay was used to measure the concentration of interleukin-1β（IL-1β）, tumor necrosis factor α, and IL-6. The dry-wet weight method was used to measure brain water content. The Evans blue dye extravasation assay was used to measure BBB disruption. Western blot assay was used to measure protein expression of nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3（NLRP3）, caspase-1 p20, IL-1β, nuclear factor kappa B（NF-κB） p65, occluding, and zonula occluden-1. Flow cytometry was used to measure cellular apoptosis. Results showed that dexmedetomidine treatment attenuated early neurological dysfunction and brain edema. Further, dexmedetomidine attenuated post-traumatic inflammation, up-regulated tight junction protein expression, and reduced secondary BBB damage and apoptosis. These protective effects were accompanied by down-regulation of the NF-κB and NLRP3 inflammasome pathways. These findings suggest that dexmedetomidine exhibits neuroprotective effects

关键词： nerve regeneration traumatic brain injury neuroinflammation nuclear factor kappa B NLRP3 inflammasome brain edema blood-brain barrier tight junction proteins apoptosis neuroprotection dexmedetomidine neural regeneration

KRAS mutation-induced EndMT of brain arteriovenous malformation is mediated through the TGF-β/BMP-SMAD4 pathway

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Stroke & Vascular Neurology 2023年第3期8卷 197-206,I0006-I0027页

作者： Hongyuan Xu Ran Huo Hao Li Yuming Jiao Jiancong Weng Jie Wang Zihan Yan Junze Zhang Shaozhi Zhao Qiheng He Yingfan Sun Shuo Wang Yong Cao department of neurosurgery Beijing Tiantan HospitalCapital medical universityBeijingChina China National Clinical Research Center for neurological Diseases BeijingChina Beijing Neurosurgical institute Capital Medical UniversityBeijingChina

Objective Somatic KRAS mutations have been identified in the majority of brain arteriovenous malformations(bAVMs),and subsequent in vivo experiments have confirmed that KRAS mutation in endothelial cells(ECs)causes AVMs in mouse and zebrafish *** previous study demonstrated that the KRASG12D mutant independently induced the endothelial-mesenchymal transition(EndMT),which was reversed by treatment with the lipid-lowering drug ***,the underlying mechanisms of action were *** We used human umbilical vein ECs(HUVECs)overexpressing the KRASG12D mutant for Western blotting,quantitative real-time PCR,and immunofluorescence and wound healing assays to evaluate the EndMT and determine the activation of downstream *** of SMAD4 by RNA interference was performed to explore the role of SMAD4 in regulating the *** ECs expressing the KRASG12D mutant were obtained to verify the SMAD4 ***,we performed a coimmunoprecipitation assay to probe the mechanism by which lovastatin affects *** HUVECs infected with KRASG12D adenovirus underwent the *** growth factor beta(TGF-β)and bone morphogenetic protein(BMP)signalling pathways were activated in the KRASG12D-mutant HUVECs and ECs in bAVM *** down SMAD4 expression in both KRASG12D-mutant HUVECs and ECs in bAVM tissues inhibited the *** attenuated the EndMT by downregulating p-SMAD2/3,p-SMAD1/5 and acetylated SMAD4 expression in KRASG12D-mutant *** Our findings suggest that the KRASG12D mutant induces the EndMT by activating the ERK-TGF-β/BMP-SMAD4 signalling pathway and that lovastatin inhibits the EndMT by suppressing TGF-β/BMP pathway activation and SMAD4 acetylation.

关键词： KRAS SMAD4 inhibited

Over-expression of nitric oxide and nitric oxide synthase in the rat brain following focal ischemia

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Neural Regeneration Research 2008年第2期3卷 162-166页

作者： Weizhong Yang Chunmei Chen Chunhua Wang Songsheng Shi Junrong Lei Yongliang Zhang department of neurosurgery Union Hospital Fujian Medical University Fujian Institute of Neurosurgery Fuzhou 350001 Fujian Province China

BACKGROUND： In cerebral ischemia, over-expression of nitric oxide （NO） exerts neurotoxic effects.OBJECTIVE： This study was designed to measure NO and nitric oxide synthase （NOS） expression in rat brain tissue during cerebral ischemia, and to correlate expression levels of NO and NOS with ischemic time. DESIGN： A complete randomized grouping design, controlled animal experiment. SETTING： Fujian institute of neurosurgery ＆ department of neurosurgery, Union Hospital Affiliated Fujian Medical University. MATERIALS： This study was performed at the Fujian institute of neurosurgery in December 2003. Eighty healthy adult male Sprague Dawley （SD） rats of clean grade were provided by the Zhejiang Laboratory Animal Center. The protocol was performed in accordance with ethical guidelines for the use and care of animals. Kits for measuring NO expression by method of nitrate reductase （Boster Company, Wuhan, China） and NOS activity （Jiancheng Bioengineering Co., Ltd., Nanjing, China）, as well as a kit for reverse transcription-PCR （RT-PCR, Promega, USA） were used in the present study. METHODS： Sixty-eight rats underwent cerebral ischemia by occluding the middle cerebral artery by suture method. Forty-eight successfully lesioned rats were included in the study. Six rats were used for each length of ischemic event （30 minutes, 1, 3, 6, 12, 24, and 72 hours, and 5 days of ischemia）. Additionally, a normal control group （n = 6, normally raised） and a sham-operated group （n = 6, corresponding cerebral vessels exposed, without occlusion of middle cerebral artery） were included in the analysis. MAIN OUTCOME MEASURES： neurological function deficits were scored according to methods of Longa, Bederson, and colleagues. NO levels and NOS activity in the brain tissue were measured via nitrate reductase and chemical colorimetry, respectively. The expression of nitrotyrosine （NT）, an in vivo specific metabolite of NO, was quantitatively measured by flow cytometry. Expression of endoth

关键词： cerebral ischemia NO eNOS, nNOS iNOS

Long-term functional outcomes improved with deep brain stimulation in patients with disorders of consciousness

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Stroke & Vascular Neurology 2023年第5期8卷 368-378页

作者： Yi Yang Qiheng He Yuanyuan Dang Xiaoyu Xia Xin Xu Xueling Chen Jizong Zhao Jianghong He department of neurosurgery Beijing Tiantan HospitalCapital Medical UniversityBeijingChina Translational Medicine Center Chinese Institute for Brain ResearchBeijingChina Beijing institute of Brain Disorders Capital Medical UniversityBeijingChina department of neurosurgery PLA General HospitalBeijingChina Academician Office China National Clinical Research Center for Neurological DiseasesBeijingChina

Background Deep brain stimulation(DBS)has been preliminarily applied to treat patients with disorders of consciousness(DoCs).The study aimed to determine whether DBS was effective for treating patients with DoC and identify factors related to patients’*** Data from 365 patients with DoCs who were consecutively admitted from 15 July 2011 to 31 December 2021 were retrospectively *** regression and subgroup analysis were performed to adjust for potential *** primary outcome was improvement in consciousness at 1 *** An overall improvement in consciousness at 1 year was achieved in 32.4%(12/37)of the DBS group compared with 4.3%(14/328)of the conservative *** full adjustment,DBS significantly improved consciousness at 1 year(adjusted OR 11.90,95%CI 3.65-38.46,p<0.001).There was a significant treatment×follow up interaction(H=14.99,p<0.001).DBS had significantly better effects in patients with minimally conscious state(MCS)compared with patients with vegetative state/unresponsive wakefulness syndrome(p for interaction<0.001).A nomogram based on age,state of consciousness,pathogeny and duration of DoCs indicated excellent predictive performance(c-index=0.882).Conclusions DBS was associated with better outcomes in patients with DoC,and the effect was likely to be significantly greater in patients with *** should be cautiously evaluated by nomogram preoperatively,and randomised controlled trials are still needed.

关键词： stimulation patients admitted

Treating supratentorial intracerebral haemorrhage: hopeless? Or rethink our strategy

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Stroke & Vascular Neurology 2021年第2期6卷 158-159页

作者： David Z Wang Liping Liu Guohua Xi Yongjun Wang Neurovascular Division Department of NeurologyBarrow Neurological InstitutePhoenixArizonaUSA department of Neurology Beijing Tiantan HospitalCapital Medical UniversityBeijingChina China National Clinical Research Center for neurological Diseases BeijingChina department of neurosurgery University of MichiganAnn ArborMichiganUSA

Intracerebral haemorrhage(ICH)is the deadliest(40%)among all strokes.1 There are about 2 million ICHs annually worldwide,but effective treatment is still *** ICH volume of<30 cm3 may have a 30-day mortality of 19%.2 Clinical research on treating ICH has been focusing on blood pressure control,haemostatic therapy,surgical evacuation of the clot and effective drainage of intraven-tricular blood.

关键词： mortality cerebral Clinical

MicroRNA and Brain Tumors

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Chinese Journal of Clinical Oncology 2007年第5期4卷 355-359,371页

作者： Xuan Zhou Chunsheng Kang Peiyu Pu department of neurosurgery Tianjin Medical University General Hospital Laboratory of Neuro-oncology Tianjin Neurological InstituteTianjin 300052 China

MicroRNAs （miRNAs） were first described in 1993 by Lee and colleagues, and the term microRNA was only introduced in 2001 in a set of three articles in Science. One of the biggest surprises in the past few years has been the emergence of miRNAs as a major new class of gene expression regulators. Recent studies suggest that miRNA alterations are involved in the initiation and progression of human cancer. The brain tumor, glioblastoma multiforme, is the most malignant and deadly form of gliomas. The prognosis is poor and the median survival with combined radiotherapy and chemotherapy is only 14.6 months. With the discovery of miRNA, the miRNA profiles may become useful biomarkers for brain tumor diagnostics, and miRNA therapy could be a powerful tool for brain tumor prevention and therapeutics. This review outlines the background of miRNA and its expression and therapeutic potential for brain tumors.

关键词： miRNA post-transcript regulation tumorigenesis cancer glioblastoma

Dural Graft-Induced Fibrotic Mass Twelve Years after Successful Treatment of Skull Base Non-Hodgkin Lymphoma Mimicking Recurrence: Case Report and Literature Review

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Open Journal of Modern neurosurgery 2014年第1期4卷 7-12页

作者： Mario Teo Sean Martin James Bowness Muftah Sam Eljamel department of neurosurgery Institute of Neurological Science Glasgow UK department of neurosurgery Ninewells Hospital Dundee UK

Non-Hodgkin lymphoma involving the skull base is a very rare tumour. The role of surgery for these patients remains controversial, as is the use of dural graft for CSF leak repair. With an increasing incidence of CNS lymphoma, more atypical presentations are reported. It is, therefore, important to include lymphoma in the differential diagnosis of skull base lesions as long-term remission is achievable for such patients, as shown in our case. Dural graft used for CSF leak repair could present with delayed complication mimicking tumour recurrence. Relevant published literature is reviewed.

关键词： CNS Lymphoma Skull Base Dural Graft Repair Delayed Complication