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Endothelial Notch activation promotes neutrophil transmigration via downregulating endomucin to aggravate hepatic ischemia/reperfusion injury

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Science China(Life Sciences) 2020年第3期63卷 375-387页

作者： Peiran Zhang kangyi yue Xinli Liu Xianchun Yan Ziyan Yang Juanli Duan Congcong Xia Xinyuan Xu Mei Zhang Liang Liang Lin Wang Hua Han State Key Laboratory of Cancer Biology Fourth Military Medical UniversityXi’an 710032China Department of Biochemistry and Molecular Biology Fourth Military Medical UniversityXi’an 710032China Department of Hepatobiliary Surgery Xijing HospitalFourth Military Medical UniversityXi’an 710032China

Inflammatory leukocytes infiltration is orchestrated by mechanisms involving chemokines,selectins,addressins and other adhesion molecules derived from endothelial cells(ECs),but how they respond to inflammatory cues and coordinate leukocyte transmigration remain *** this study,using hepatic ischemia/reperfusion injury(HIRI)as a model,we identified that endothelial Notch activation was rapidly and dynamically induced in liver sinusoidal endothelial cells(LSECs)in acute *** mice with EC-specific Notch activation(NICeCA),HIRI induced exacerbated liver ***,endothelial Notch activation enhanced neutrophil infiltration and tumor necrosis factor(TNF)-αexpression in *** analysis and further qRT-PCR as well as immunofluorescence indicated that endomucin(EMCN),a negative regulator of leukocyte adhesion,was downregulated in LSECs from NICeCA *** was downregulated during HIRI in wild-type mice and in vitro cultured ECs insulted by hypoxia/re-oxygenation *** activation in ECs led to increased neutrophil adhesion and transendothelial migration,which was abrogated by EMCN overexpression in *** mice deficient of RBPj,the integrative transcription factor of canonical Notch signaling,although overwhelming sinusoidal malformation aggravated HIRI,the expression of EMCN was upregulated;and pharmaceutical Notch blockade in vitro also upregulated EMCN and inhibited transendothelial migration of *** Notch activation-exaggerated HIRI was compromised by blocking LFA-1,which mediated leukocyte adherence by associating with ***,endothelial Notch signaling controls neutrophil transmigration via EMCN to modulate acute inflammation in HIRI.

关键词： leukocyte transendothelial migration hepatic ischemia/reperfusion injury(HIRI) liver sinusoidal endothelial cells(LSECs) Notch endomucin(EMCN)

脑缺血模型中皮层Sirt3与自噬蛋白LC3表达的相关性

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中华神经外科疾病研究杂志 2018年第5期17卷 387-390页

作者：李建荣蒋晓帆张磊岳康异黑悦空军军医大学西京医院神经外科陕西西安710032

目的观察小鼠脑缺血再灌注损伤模型中皮层区域沉默信息因子3(SIRT3)和自噬相关蛋白LC3的表达,并探讨两者的相关性。方法使用C57BL/6J小鼠大脑中动脉阻塞(MCAO)建立缺血再灌注损伤模型,并随机分为4组(即再灌注3 h、24 h、3 d和7 d组),应... 详细信息

目的观察小鼠脑缺血再灌注损伤模型中皮层区域沉默信息因子3(SIRT3)和自噬相关蛋白LC3的表达,并探讨两者的相关性。方法使用C57BL/6J小鼠大脑中动脉阻塞(MCAO)建立缺血再灌注损伤模型,并随机分为4组(即再灌注3 h、24 h、3 d和7 d组),应用间接免疫荧光和蛋白印迹法观察缺血再灌注不同时间点小鼠大脑皮层损伤区SIRT3和LC3的表达,后使用Spearman相关性分析比较两者的相关性。结果免疫荧光结果发现SIRT3术后呈现动态高表达,并于再灌注24 h达到高峰,整体随时间呈现抛物线状变化,而LC3与SIRT3变化趋势基本相同,且存在共定位表达;蛋白印迹实验结果进一步验证了SIRT3和LC3的相似表达趋势,Spearman相关性分析发现两者表达趋势具有显著相关性(P <0. 05)。结论小鼠脑缺血再灌注损伤大脑皮层SIRT3和LC3的表达具有显著相关性,SIRT3对自噬的调节可能有重要作用。

关键词：沉默信息调节因子3 微观相关蛋白3 自噬脑缺血皮层

Sirtuin 3在中枢神经系统退行性疾病中的研究进展

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空军军医大学学报 2024年第4期45卷 455-460页

作者：张昊阜子岳康异邹鹏罗鹏蒋晓帆空军军医大学西京医院神经外科陕西西安710032

Sirtuin 3(Sirt3)是一种烟酰胺腺嘌呤二核苷酸依赖的蛋白脱乙酰基酶,主要参与线粒体代谢过程,包括能量合成、三羧酸循环和氧化应激。更多的科学研究证实,Sirt3具有抗氧化应激、抗细胞凋亡以及保持代谢稳态的作用,在能量代谢、肿瘤、衰... 详细信息

Sirtuin 3(Sirt3)是一种烟酰胺腺嘌呤二核苷酸依赖的蛋白脱乙酰基酶,主要参与线粒体代谢过程,包括能量合成、三羧酸循环和氧化应激。更多的科学研究证实,Sirt3具有抗氧化应激、抗细胞凋亡以及保持代谢稳态的作用,在能量代谢、肿瘤、衰老等过程中起着重要作用。最近的研究发现,在神经退行性疾病中,Sirt3激活可以减缓或抑制线粒体功能障碍,从而显示出显著的神经保护作用。本文综述了Sirt3在神经退行性疾病中的保护作用及其可能机制。

关键词： Sirtuin3 阿尔茨海默症帕金森病亨廷顿病肌萎缩侧索硬化症多发性硬化症中枢神经系统

Curcumin in gastric cancer treatment:A commentary on mechanistic insights and future directions

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World Journal of Gastrointestinal Oncology 2025年第1期17卷 265-267页

作者： Xin-yue Wei Wen-Bo Cao Sai-Jun Mo Zhi-Yan Sun Department of Pathophysiology School of Basic Medical SciencesZhengzhou UniversityZhengzhou 450001Henan ProvinceChina School of Basic Medical Science Zhengzhou UniversityZhengzhou 450001Henan ProvinceChina Department of Basic Science of Oncology School of Basic Medical SciencesZhengzhou UniversityZhengzhou 450001Henan ProvinceChina Department of Special Service No.988 Hospital of the Joint Service Support Force of PLAZhengzhou 450042Henan ProvinceChina

The study by Yang et al presents a comprehensive investigation into the thera-peutic potential of curcumin for gastric cancer(GC).Using network pharma-cology,the researchers identified 48 curcumin-related genes,31 of which overlap with GC *** genes,including ESR1,EGFR,CYP3A4,MAPK14,CYP1A2,and CYP2B6,are linked to poor survival in GC *** docking con-firmed strong binding affinity of curcumin to these *** vitro experiments demonstrated that curcumin effectively inhibits the growth and proliferation of BGC-823,suggesting its therapeutic potential in GC through multiple targets and pathways.

关键词： Curcumin Gastric cancer Network pharmacology Mechanism of action In vitro experiments

PINK1介导的线粒体自噬在小鼠皮层神经元氧糖剥夺后表达和意义

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中华神经外科疾病研究杂志 2018年第2期17卷 143-146页

作者：王元欣张磊黑悦鱼洋岳康异武秀权蒋晓帆空军军医大学西京医院神经外科陕西西安710032 扶风县人民医院神经外科陕西宝鸡722200

目的探究不同时长氧糖剥夺(OGD)后小鼠皮层神经元中线粒体自噬相关蛋白PTEN诱导的假定激酶1(PINK1)表达的时空动态改变。方法 C57BL/6J小鼠皮层神经元原代培养7 d,以OGD不同时长(0 h、2 h、4 h、6 h、8 h)作为观察时间点。倒置显微镜下... 详细信息

目的探究不同时长氧糖剥夺(OGD)后小鼠皮层神经元中线粒体自噬相关蛋白PTEN诱导的假定激酶1(PINK1)表达的时空动态改变。方法 C57BL/6J小鼠皮层神经元原代培养7 d,以OGD不同时长(0 h、2 h、4 h、6 h、8 h)作为观察时间点。倒置显微镜下观察神经元形态变化;MTT比色法检测神经元存活率;蛋白印迹法(Western blot,WB)观察LC3-Ⅱ、PINK1和Parkin表达的时间变化;免疫荧光观察PINK1OGD后表达的空间改变。结果 OGD严重损伤神经元活性,且随着时间延长细胞活性呈进展性下降趋势;OGD后自噬标志性分子LC3-Ⅱ和PINK1开始升高(4 h达到峰值)(P<0.05),后进行性下降,而Parkin表达逐渐下降(P<0.05);PINK1在胞浆可见均匀表达,在OGD后荧光强度短暂增高,并随OGD时间逐渐减弱。结论不同时长OGD可造成不同程度神经元损伤,并激活PINK1介导的线粒体自噬,PINK1可能通过影响线粒体在脑缺血损伤的病理生理过程中发挥作用。

关键词：同源性磷酸酶-张力蛋白诱导的激酶1 微管相关蛋白1轻链3 氧糖剥夺神经元线粒体自噬

帕金森病细胞模型中维生素C调控SIRT3影响自噬水平的研究

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中华神经外科疾病研究杂志 2018年第5期17卷 432-435页

作者：王元欣岳康异鱼洋武秀权孙季冬张磊扶风县人民医院神经外科陕西宝鸡722200 空军军医大学西京医院神经外科陕西西安710032

目的探讨维生素C(Vit C)通过调控沉默信息调解转录因子3(SIRT3)影响帕金森病模型中PC12细胞自噬的意义和作用机制。方法培养拟神经元PC12细胞株,随机分组为:正常对照组(Control组)、单纯Vit C组(Vit C组)、帕金森病组(MPP^+组)和Vit C... 详细信息

目的探讨维生素C(Vit C)通过调控沉默信息调解转录因子3(SIRT3)影响帕金森病模型中PC12细胞自噬的意义和作用机制。方法培养拟神经元PC12细胞株,随机分组为:正常对照组(Control组)、单纯Vit C组(Vit C组)、帕金森病组(MPP^+组)和Vit C治疗组(Vit C+MPP^+组),在含有Vit C组中分别加入400μmol/L Vit C孵育6 h后,在含有MPP^+组中均加入700μmol/L MPP^+,模拟帕金森病的神经细胞损伤,孵育48 h后,利用细胞增殖-毒性检测试剂盒(cell counting Kit-8,CCK-8)检测细胞存活率;利用小鼠乳酸脱氢酶(LDH)试剂盒检测LDH变化; Western blot(WB)检测PC12细胞中SIRT3、微管相关蛋白1轻链3(LC3-Ⅱ)的表达变化情况,免疫荧光检测细胞SIRT3、LC3-Ⅱ的表达变化情况。结果 CCK-8和LDH检测结果提示,Vit C能改善细胞生存环境,明显减轻帕金森病PC12细胞损伤,提高细胞活力;同样的,WB结果提示,与MPP^+组比较,Vit C上调SIRT3和LC3-Ⅱ的表达,促进神经元自噬的发生,组间差异有统计学意义(P <0. 05);同样的,免疫荧光结果显示,Vit C+MPP^+组中SIRT3和LC3-Ⅱ荧光强度均较MPP^+组增加。结论 Vit C可以激活SIRT3表达,并提高细胞自噬,发挥一种内源性的神经保护作用,拮抗MPP^+对PC12细胞的损伤。

关键词：帕金森病沉默信息调解转录因子3 维生素C PC12细胞自噬

Pulp health and calcific healing of a complicated crown–root fracture with additional root fracture in a maxillary incisor: A case report

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World Journal of Clinical Cases 2025年第3期13卷 42-49页

作者： Na Li yue-yue Ren Ying Tang Qi Yang Tian-Tian Meng Song Li Jing Zhang Stomatological Hospital and College Anhui Medical UniversityHefei 230032Anhui ProvinceChina Department of Endodontics The Affiliated Stomatological Hospital of Xuzhou Medical UniversityXuzhou 221000Jiangsu ProvinceChina

BACKGROUND Complicated crown–root fracture (CRF) involves severe injury to the crown, root,and pulp, and may be accompanied by multiple root fractures. The loss of a toothhas lifelong consequences for children and teenagers, but the maintenance of pulphealth and the calcific healing of multiple root fractures are rarely reported in *** SUMMARY This case reports healing of a permanent tooth with complicated crown–root andadditional root fractures, in which pulp health was maintained. A 10-year-old girlfell and fractured the root of her maxillary left central incisor at the cervical *** the coronal fragment was repositioned, the tooth was splinted until thetooth was no longer mobile, 2 years later. Eight years after treatment, the toothhas remained asymptomatic with vital pulp and localized gingival ***-beam computed tomography revealed not only calcified healing of the CRFbut also spontaneous healing in an additional undiagnosed root fracture. Thefracture line on the enamel could not be healed by hard tissue and formed agroove in the cervical crown. It was speculated that the groove was related to thelocalized gingival *** This case provides a clinical perspective of the treatment of a tooth with acomplicated CRF and an additional root fracture.

关键词： Complicated crown-root fracture Multiple root fracture Spontaneous healing Cone-beam computed tomography Long-term follow-up Case report

Inhibition of the cGAS–STING pathway:contributing to the treatment of cerebral ischemia-reperfusion injury

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Neural Regeneration Research 2025年第7期20卷 1900-1918页

作者： Hang Yang Yulei Xia yue Ma Mingtong Gao Shuai Hou Shanshan Xu Yanqiang Wang School of Clinical Medicine Shandong Second Medical UniversityWeifangShandong ProvinceChina Department of Emergency The Affiliated Hospital of Weifang Medical UniversityWeifangShandong ProvinceChina Department of Neurology Ⅱ The Affiliated Hospital of Weifang Medical UniversityWeifangShandong ProvinceChina

The cGAS–STING pathway plays an important role in ischemia-reperfusion injury in the heart,liver,brain,and kidney,but its role and mechanisms in cerebral ischemia-reperfusion injury have not been systematically ***,we outline the components of the cGAS–STING pathway and then analyze its role in autophagy,ferroptosis,cellular pyroptosis,disequilibrium of calcium homeostasis,inflammatory responses,disruption of the blood–brain barrier,microglia transformation,and complement system activation following cerebral ischemia-reperfusion *** further analyze the value of cGAS–STING pathway inhibitors in the treatment of cerebral ischemia-reperfusion injury and conclude that the pathway can regulate cerebral ischemia-reperfusion injury through multiple *** of the cGAS–STING pathway may be helpful in the treatment of cerebral ischemia-reperfusion injury.

关键词： calcium homeostasis cellular autophagy cerebral ischemia-reperfusion injury cGAS–STING pathway ferroptosis gut–brain–microbiota axis inflammatory light chain 3 microglial cells Syntaxin-17 protein

1990年-2019年亚洲主要国家中枢神经系统恶性肿瘤疾病负担研究及相关预测

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国际神经病学神经外科学杂志 2024年第5期51卷 83-90页

作者：葛俊苗孙季冬张昊阜子葛俊丽岳康异蒋晓帆罗鹏空军军医大学第一附属医院神经外科陕西西安710032 空军军医大学第一附属医院妇产科陕西西安710032

目的分析亚洲主要国家中枢神经系统(CNS)恶性肿瘤的疾病负担,预测中国CNS恶性肿瘤未来流行趋势。方法基于2019年全球疾病负担研究数据,收集全球及亚洲主要国家的CNS恶性肿瘤疾病负担数据,分析年份、社会人口指数对CNS恶性肿瘤发病、患... 详细信息

目的分析亚洲主要国家中枢神经系统(CNS)恶性肿瘤的疾病负担,预测中国CNS恶性肿瘤未来流行趋势。方法基于2019年全球疾病负担研究数据,收集全球及亚洲主要国家的CNS恶性肿瘤疾病负担数据,分析年份、社会人口指数对CNS恶性肿瘤发病、患病、失能调整生命年(DALYs)、死亡等指标的变化趋势,采用估计年百分比变化(EAPC)及其95%置信区间(CI)描述标化率的趋势。分析中国2019年不同性别、年龄组CNS恶性肿瘤疾病负担,采用NORPRED模型预测2020年-2044年中国CNS恶性肿瘤发病和死亡情况。结果亚洲主要国家中,日本疾病负担最重,标化发病率、患病率、DALYs率和死亡率的EAPC分别为:2.28%(95%CI:1.94%~2.62%),2.65%(95%CI:2.24%~3.06%),1.02%(95%CI:0.87%~1.18%)和1.46%(95%CI:1.29%~1.64%)。1990年-2019年,中国CNS恶性肿瘤的标化发病率从4.45/10万上升至5.69/10万,标化患病率从8.15/10万上升至22.58/10万,标化DALYs率从161.29/10万下降至126.24/10万,标化死亡率从3.87/10万下降至3.50/10万。2019年,中国女性CNS恶性肿瘤发病率、患病率高于男性,男性死亡率高于女性,DALYs率两者差别不大。NORDPRED模型预测结果显示,中国CNS恶性肿瘤标化发病率在2020年-2044年呈连续上升趋势,预计增长26.65%,标化死亡率将有所下降,预计下降9.14%。结论相较于韩国和日本,中国CNS恶性肿瘤疾病负担虽有所改善,但在全球仍处于较高水平。85岁以上老年人疾病负担最重,尤其是男性,需重点关注。

关键词：中枢神经系统恶性肿瘤发病率患病率死亡率失能调整生命年疾病负担预测