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Neuroscience Bulletin 2020年第10期36卷 1158-1170页

作者： Xun Wu Wenxing Cui Wei Guo Haixiao Liu Jianing Luo Lei Zhao Hao Guo Longlong Zheng Hao Bai Dayun Feng Yan Qu Department of Neurosurgery Tangdu HospitalFourth Military Medical UniversityXi'an 710038China

Clinical advances in the treatment of intracranial hemorrhage(ICH)are restricted by the incomplete understanding of the molecular mechanisms contributing to secondary brain *** is a highly active unsaturated aldehyde which has been implicated in many nervous system *** results indicated a significant increase in the level of acrolein after ICH in mouse *** primary neurons,acrolein induced an increase in mitochondrial fragmentation,loss of mitochondrial membrane potential,generation of reactive oxidative species,and release of mitochondrial cytochrome ***,acrolein facilitated the translocation of dynaminrelated protein 1(Drpl)from the cytoplasm onto the mitochondrial membrane and led to excessive mitochondrial *** studies found that treatment with hydralazine(an acrolein scavenger)significantly reversed Drpl translocation and the morphological damage of mitochondria after *** parallel,the neural apoptosis,brain edema,and neurological functional deficits induced by ICH were also remarkably *** conclusion,our results identify acrolein as an important contributor to the secondary brain injury following ***,we uncovered a novel mechanism by which Drpl-mediated mitochondrial oxidative damage is involved in acroleininduced brain injury.

关键词： Intracerebral hemorrhage secondary brain injury Acrolein Drp1 Mitochondrial oxidative damage

Changes in platelet parameters and secondary brain injury in acute craniocerebral trauma

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Neural Regeneration Research 2011年第20期6卷 1543-1547页

作者： Xiaoping Tang Chao You Hua Peng Tao Zhang Wenguo Tang Jian Qi Renguo Luo Yuanchuan Wang Ling Feng Zhangyang Gou Junwei Duan Shun Li Department of Neurosurgery West China Hospital Sichuan University Chengdu 610041 Sichuan Province China Department of Neurosurgery Affiliated Hospital of North Sichuan Medical College Nanchong 637000 Sichuan Province China

Changes in platelet parameters are important in secondary brain injury in acute craniocerebral trauma We selected 163 patients with craniocerebral trauma who were admitted within 24 hours with nonoperative therapy. Platelet parameters of 40 healthy subjects served as controls. Platelet number was decreased, while mean platelet volume and platelet distribution width values were increased, at 1 and 3 days after injury. Platelet number was lower and mean platelet volume and platelet distribution width were larger in patients with traumatic cerebral infarction and those in Glasgow Coma Scale score 〈 8 group. Platelet number was negatively correlated to volume of cerebral edema, but positively correlated to Glasgow Outcome Scale score. These data indicate that changes in platelet parameters may be utilized to indicate the state of central nervous system injury and patient prognosis .

关键词： craniocerebral trauma platelet mean platelet volume platelet distribution width secondary brain injury

Changes in circulating inflammatory cells and the relationship to secondary brain injury in patients with craniocerebral injury

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Neural Regeneration Research 2008年第8期3卷 867-870页

作者： Xiaoping Tang Tao Zhang Yuanchuan Wang Hua Peng Ling Feng Jian Qi Wenguo Tang Zhangyang Gou Dingyong Yu Renguo Luo Department of Neurosurgery Affiliated Hospital of North Sichuan Medical University Nanchong 637000 Sichuan Province China

BACKGROUND：Recent studies have indicated that reactive encephalitis plays an important role in secondary tissue damage after craniocerebral injury. OBJECTIVE： To observe changes in white blood cells （WBC） and polymorphonuclear neutrophils （PMN） in peripheral blood, and to determine their role in secondary brain insult in patients with craniocerebral injury. DESIGN, TIME AND SETTING： A case-control study at the Department of Neurosurgery of the Affiliated Hospital North Sichuan University of Medical Sciences between August 2007 and May 2008. PARTICIPANTS： Sixty-three patients, admitted within 24 hours after craniocerebral injury and who received no surgery, were included in the study. The cohort consisted of 41 males and 22 females, aged 9–72 years, with an average age of 42 years. Ten healthy volunteers, selected from the Department of Neurosurgery, were designated as the control group. METHODS： WBC and PMN from the peripheral blood were measured 0, 24, 48, 72, and 168 hours after admission to hospital. The Glasgow coma scale, area of cerebral hemorrhage, and degree of brain edema were simultaneously determined. The Glasgow outcome scale was evaluated six months after injury. The relationship between changes in WBC and PMN were analyzed. Sixty-three patients were divided into 0, 24, 48, 72, and 168 hours groups, with admission time to hospital as the determining factor. As controls, WBC and PMN of peripheral blood were also detected in 10 healthy volunteers. MAIN OUTCOME MEASURES： The main outcome measures were WBC and PMN counts in the peripheral blood at 0, 24, 48, 72, and 168 hours after admission to hospital, the mutual relationship between GCS, WBC and PMN, and changes in brain hemorrhage volume and edema size. RESULTS： WBC peaked at 24 hours after injury, and PMN peaked at 48 hours after injury （P 〈 0.01）. These measures negatively correlated to the Glasgow coma scale （r = -0.657, -0.541, respectively, P 〈 0.05）. In patients with Glasgow coma sale 〈 8, WBC and

关键词： craniocerebral injury inflammatory cells secondary brain injury

Mitophagy in intracerebral hemorrhage:a new target for therapeutic intervention

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Neural Regeneration Research 2024年第2期19卷 316-323页

作者： Yiyang Chen Wenxuan Tang Xinqi Huang Yumei An Jiawen Li Shengye Yuan Haiyan Shan Mingyang Zhang Institute of Forensic Sciences Suzhou Medical CollegeSoochow UniversitySuzhouJiangsu ProvinceChina Shanghai Key Lab of Forensic Medicine Key Lab of Forensic ScienceMinistry of Justice(Academy of Forensic Science)ShanghaiChina Department of Obstetrics and Gynecology The Affiliated Suzhou Hospital of Nanjing Medical UniversitySuzhouJiangsu ProvinceChina

Intracerebral hemorrhage is a life-threatening condition with a high fatality rate and severe ***,there is currently no treatment available for intracerebral hemorrhage,unlike for other stroke *** studies have indicated that mitochondrial dysfunction and mitophagy likely relate to the pathophysiology of intracerebral ***,or selective autophagy of mitochondria,is an essential pathway to preserve mitochondrial homeostasis by clearing up damaged *** markedly contributes to the reduction of secondary brain injury caused by mitochondrial dysfunction after intracerebral *** review provides an overview of the mitochondrial dysfunction that occurs after intracerebral hemorrhage and the underlying mechanisms regarding how mitophagy regulates it,and discusses the new direction of therapeutic strategies targeting mitophagy for intracerebral hemorrhage,aiming to determine the close connection between mitophagy and intracerebral hemorrhage and identify new therapies to modulate mitophagy after intracerebral *** conclusion,although only a small number of drugs modulating mitophagy in intracerebral hemorrhage have been found thus far,most of which are in the preclinical stage and require further investigation,mitophagy is still a very valid and promising therapeutic target for intracerebral hemorrhage in the long run.

关键词： intracerebral hemorrhage mitochondrial dysfunction mitophagy neuroinflammation neuroprotection reactive oxygen species secondary brain injury therapeutic target

Inhibition of endoplasmic reticulum stress alleviates secondary injury after traumatic brain injury

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Neural Regeneration Research 2018年第5期13卷 827-836页

作者： Hong-Ping Tan Qiang Guo Gang Hua Jun-Xi Chen Jun-Chao Liang Southern Medical University Guangzhou Guangdong Province China Department of Epilepsy Surgery Guangdong Sanjiu Brain Hospital Guangzhou Guangdong Province China Department of Neurosurgery Guangzhou General Hospital of Guangzhou Military Command Guangzhou Guangdong Province China

Apoptosis after traumatic brain injury has been shown to be a major factor influencing prognosis and outcome. Endoplasmic reticulum stress may be involved in mitochondrial mediated neuronal apoptosis. Therefore, endoplasmic reticulum stress has become an important mechanism of secondary injury after traumatic brain injury. In this study, a rat model of traumatic brain injury was established by lateral fluid percussion injury. Fluorescence assays were used to measure reactive oxygen species content in the cerebral cortex. Western blot assays were used to determine expression of endoplasmic reticulum stress-related proteins. Hematoxylin-eosin staining was used to detect pathological changes in the cerebral cortex. Transmission electron microscopy was used to measure ultrastructural changes in the endoplasmic reticulum and mitochondria. Our results showed activation of the endoplasmic reticulum stress-related unfolded protein response. Meanwhile, both the endoplasmic reticulum stress response and mitochondrial apoptotic pathway were activated at different stages post-traumatic brain injury. Furthermore, pretreatment with the endoplasmic reticulum stress inhibitor, salubrinal（1 mg/kg）, by intraperitoneal injection 30 minutes before injury significantly inhibited the endoplasmic reticulum stress response and reduced apoptosis. Moreover, salubrinal promoted recovery of mitochondrial function and inhibited activation of the mitochondrial apoptotic pathway post-traumatic brain injury. These results suggest that endoplasmic reticulum stress might be a key factor for secondary brain injury post-traumatic brain injury.

关键词： nerve regeneration traumatic brain injury endoplasmic reticulum stress apoptosis mitochondria reactive oxygen species unfolded protein response secondary brain injury salubrinal neural regeneration

Oxidized low-density lipoprotein receptor 1:a novel potential therapeutic target for intracerebral hemorrhage

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Neural Regeneration Research 2022年第8期17卷 1795-1801页

作者： Hui-Yuan Zhang Xi Lu Yue-Han Hao Ling Tang Zhi-Yi He Department of Neurology The First Hospital of China Medical UniversityShenyangLiaoning ProvinceChina

Oxidized low-density lipoprotein receptor 1(OLR1)is upregulated in neurons and participates in hypertension-induced neuronal ***1 deletion exerts protective effects on cerebral damage induced by hypertensive-induced ***,OLR1 is likely involved in the progress of intracerebral *** this study,we examined the potential role of OLR1 in intracerebral hemorrhage using a rat ***1 small interfering RNA(10μL;50 pmol/μL)was injected into the right basal ganglia to knock down ***-four hours later,0.5 U collagenase type VII was injected to induce intracerebral *** found that knockdown of OLR1 attenuated neurological behavior impairment in rats with intracerebral hemorrhage and reduced hematoma,neuron loss,inflammatory reaction,and oxidative stress in rat brain *** also found that silencing of OLR1 suppressed ferroptosis induced by intracerebral hemorrhage and the p38 signaling ***,silencing OLR1 exhibits protective effects against secondary injury of intracerebral *** findings suggest that OLR1 may be a novel potential therapeutic target for intracerebral hemorrhage.

关键词： ferroptosis inflammation intracerebral hemorrhage neurological behavior neuroprotection novel therapeutic target oxidative stress oxidized low-density lipoprotein receptor 1 p38 signaling pathway secondary brain injury

Myeloperoxidase: a new target for the treatment of stroke?

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Neural Regeneration Research 2022年第8期17卷 1711-1716页

作者： Yun-Chang Wang Yu-Bao Lu Xiao-Lan Huang Yong-Feng Lao Lu Zhang Jun Yang Mei Shi Hai-Long Ma Ya-Wen Pan Yi-Nian Zhang The Second Clinical Medical School Lanzhou UniversityLanzhouGansu ProvinceChina Department of Neurosurgery Lanzhou University Second HospitalLanzhouGansu ProvinceChina Xiangya Hospital Central South UniversityChangshaHunan ProvinceChina Department of Spine Surgery The Third Affiliated HospitalSun Yat-sen UniversityGuangzhouGuangdong ProvinceChina University of Chinese Academy of Sciences BeijingChina

Myeloperoxidase is an important inflammatory factor in the myeloid system,primarily expressed in neutrophils and *** and its active products participate in the occurrence and development of hemorrhagic and ischemic stroke,including damage to the blood-brain barrier and *** a specific inflammatory marker,myeloperoxidase can be used in the evaluation of vascular disease occurrence and development in stroke,and a large amount of experimental and clinical data has indicated that the inhibition or lack of myeloperoxidase has positive impacts on stroke *** studies have also shown that there is a correlation between the overexpression of myeloperoxidase and the risk of *** occurrence of stroke not only refers to the first occurrence but also includes ***,myeloperoxidase is significant for the clinical evaluation and prognosis of *** paper reviews the potential role played by myeloperoxidase in the development of vascular injury and secondary brain injury after stroke and explores the effects of inhibiting myeloperoxidase on stroke *** paper also analyzes the significance of myeloperoxidase etiology in the occurrence and development of stroke and discusses whether myeloperoxidase can be used as a target for the treatment and prediction of stroke.

关键词： blood-brain barrier hemorrhagic stroke inflammation ischemic stroke microglia myeloperoxidase neutrophils secondary brain injury stroke

Neutrophil-derived interleukin-17A participates in neuroinflammation induced by traumatic brain injury

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Neural Regeneration Research 2023年第5期18卷 1046-1051页

作者： Xiao-Jian Xu Qian-Qian Ge Meng-Shi Yang Yuan Zhuang Bin Zhang Jin-Qian Dong Fei Niu Hao Li Bai-Yun Liu Beijing Key Laboratory of Central Nervous System injury Beijing Neurosurgical InstituteCapital Medical UniversityBeijingChina Beijing Key Laboratory of Central Nervous System injury and Department of Neurosurgery Beijing Neurosurgical Institute and Beijing Tiantan HospitalCapital Medical UniversityBeijingChina Nerve injury and Repair Center of Beijing Institute for brain Disorders BeijingChina China National Clinical Research Center for Neurological Diseases BeijingChina

After brain injury, infiltration and abnormal activation of neutrophils damages brain tissue and worsens inflammation, but the mediators that connect activated neutrophils with neuroinflammation have not yet been fully clarified. To identify regulators of neutrophil-mediated neuroinflammation after traumatic brain injury, a mouse model of traumatic brain injury was established by controlled cortical impact. At 7 days post-injury(sub-acute phase), genome-wide transcriptomic data showed that interleukin 17 A-associated signaling pathways were markedly upregulated, suggesting that interleukin 17 A may be involved in neuroinflammation. Double immunofluorescence staining showed that interleukin 17 A was largely secreted by neutrophils rather than by glial cells and neurons. Furthermore, nuclear factor-kappaB and Stat3, both of which are important effectors in interleukin 17 A-mediated proinflammatory responses, were significantly activated. Collectively, our findings suggest that neutrophil-derived interleukin 17 A participates in neutrophil-mediated neuroinflammation during the subacute phase of traumatic brain injury. Therefore, interleukin 17 A may be a promising therapeutic target for traumatic brain injury.

关键词： immune infiltration innate immunity interleukin-17A neurodegenerative disease neuroinflammation neutrophils secondary brain injury transcription factor transcriptome traumatic brain injury

Knockdown of NADPH oxidase 4 reduces mitochondrial oxidative stress and neuronal pyroptosis following intracerebral hemorrhage

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Neural Regeneration Research 2023年第8期18卷 1734-1742页

作者： Bo-Yun Ding Chang-Nan Xie Jia-Yu Xie Zhuo-Wei Gao Xiao-Wei Fei En-Hui Hong Wen-Jin Chen Yi-Zhao Chen Guangdong Provincial Key Laboratory on brain Function Repair and Regeneration Department of NeurosurgeryZhujiang HospitalThe National Key Clinical SpecialtyThe Neurosurgery Institute of Guangdong ProvinceThe Engineering Technology Research Center of Education Ministry of ChinaSouthern Medical UniversityGuangzhouGuangdong ProvinceChina Department of Spinal Surgery Orthopedic Medical CenterZhujiang HospitalSouthern Medical UniversityGuangzhouGuangdong ProvinceChina Department of Traditional Chinese Medicine The Third Affiliated Hospital of Southern Medical UniversityGuangzhouGuangdong ProvinceChina Department of Neurosurgery Xijing HospitalAir Force Military Medical UniversityXi’anShaanxi ProvinceChina Department of Neurosurgery Peking University Shenzhen HospitalShenzhen Peking University-The Hong Kong University of Science and Technology Medical CenterShenzhenGuangdong ProvinceChina Department of Neurosurgery The First Affiliated Hospital of Guangzhou Medical UniversityGuangzhou Medical UniversityGuangzhouGuangdong ProvinceChina

Intracerebral hemorrhage is often accompanied by oxidative stress induced by reactive oxygen species,which causes abnormal mitochondrial function and secondary reactive oxygen species *** creates a vicious cycle leading to reactive oxygen species accumulation,resulting in progression of the pathological ***,breaking the cycle to inhibit reactive oxygen species accumulation is critical for reducing neuronal death after intracerebral *** previous study found that increased expression of nicotinamide adenine dinucleotide phosphate oxidase 4(NADPH oxidase 4,NOX4)led to neuronal apoptosis and damage to the blood-brain barrier after intracerebral *** purpose of this study was to investigate the role of NOX4 in the circle involving the neuronal tolerance to oxidative stress,mitochondrial reactive oxygen species and modes of neuronal death other than apoptosis after intracerebral *** found that NOX4 knockdown by adeno-associated virus(AAV-NOX4)in rats enhanced neuronal tolerance to oxidative stress,enabling them to better resist the oxidative stress caused by intracerebral *** of NOX4 also reduced the production of reactive oxygen species in the mitochondria,relieved mitochondrial damage,prevented secondary reactive oxygen species accumulation,reduced neuronal pyroptosis and contributed to relieving secondary brain injury after intracerebral hemorrhage in ***,we used a mitochondria-targeted superoxide dismutase mimetic to explore the relationship between reactive oxygen species and *** mitochondria-targeted superoxide dismutase mimetic inhibited the expression of NOX4 and neuronal pyroptosis,which is similar to the effect of *** indicates that NOX4 is likely to be an important target for inhibiting mitochondrial reactive oxygen species production,and NOX4 inhibitors can be used to alleviate oxidative stress response induced by intracerebral hemorrhage.

关键词： caspase 1 caspase4/11 gasdermin D intracerebral hemorrhage mitochondria reactive oxygen species inhibitor NADPH oxidase 4 neuronal pyroptosis neuronal tolerance reactive oxygen species secondary brain injury