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| 1 | 脊髓继发性损伤大鼠脊髓组织中丙烯醛表达、SOD活性及MDA含量变化显示文摘目的观察脊髓继发性损伤大鼠脊髓组织中丙烯醛(ACR)表达、超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量变化。方法健康雄性SD大鼠48只,随机分为实验组30只、假手术组18只。实验组采用改良Allen's-WD法制备大鼠脊髓继发性损伤模型,假手术组暴露脊髓后立即缝合。分别于建模后24 h、3 d、7 d处死大鼠,取脊髓组织,HE染色观察脊髓组织病理变化,采用免疫组化法检测脊髓组织中的ACR,采用黄嘌呤氧化酶法检测SOD活性,硫代巴比妥酸法检测MDA。结果实验组建模后24 h、3 d、7 d脊髓组织中ACR表达量、MDA含量高于相应时点假手术组(P均<0.05)。实验组建模后24 h、3 d、7 d脊髓组织SOD活性低于假手术组(P均<0.01)。结论大鼠脊髓继发性损伤组织中ACR表达及MDA含量升高,SOD活性降低。 | 张月娥 许灿 蔺静 黄一茜 张静 | 2015 | 山东医药2015，55，39： | 8 |
| 2 | 神经干细胞移植对大鼠脊髓损伤后Caspase-3和c-fos表达的影响显示文摘目的研究神经干细胞移植对大鼠脊髓损伤后Caspase-3和c-fos表达的影响。方法 SD大鼠45只,随机分成3组(n=15):假手术组、脊髓损伤模型组(模型组)和神经干细胞移植组。假手术组仅打开锥板但不离断脊髓;模型组动物锥板打开后横向断开脊髓,止血并逐层缝合;神经干细胞移植组椎板打开后横向断开脊髓,止血并注入神经干细胞悬液,再逐层缝合。手术后1、2、3和14 d对大鼠进行神经功能评分(BBB评分)。14 d后处死动物,取脊髓组织,部分用于制备切片并进行TUNEL标记,检测神经细胞(神经元)的凋亡;对另一部分脊髓组织进行蛋白提取,Western blotting检测Caspase-3和c-fos蛋白的表达。结果与假手术组相比,模型组和神经干细胞移植组BBB评分均显著下降(P<0.05);但神经干细胞移植组神经功能改善情况好于模型组(P<0.05)。模型组和神经干细胞移植组的细胞凋亡率均显著高于假手术组(P<0.05);神经干细胞移植组细胞凋亡率明显低于模型组(P<0.05)。Western blotting检测结果显示,模型组和神经干细胞移植组大鼠脊髓组织中Caspase-3和c-fos的表达量显著高于假手术组(P<0.05);神经干细胞移植组大鼠脊髓组织中Caspase-3和c-fos的表达量显著低于模型组(P<0.05)。结论在大鼠脊髓损伤后,神经干细胞移植能够加快大鼠损伤后的恢复并降低细胞凋亡率,使Caspase-3和c-fos的表达量减少,对大鼠脊髓损伤具有治疗作用。 | 刘畅 陈晓 李诚 乔苏迟 朱德刚 吾不力.阿扎提 苏佳灿 王志伟 | 2015 | 上海交通大学学报(医学版)2015，35，3： | 5 |
| 3 | Acrolein Aggravates Secondary Brain Injury After Intracerebral Hemorrhage Through Drp1-Mediated Mitochondrial Oxidative Damage in Mice显示文摘Clinical advances in the treatment of intracranial hemorrhage(ICH)are restricted by the incomplete understanding of the molecular mechanisms contributing to secondary brain injury.Acrolein is a highly active unsaturated aldehyde which has been implicated in many nervous system diseases.Our results indicated a significant increase in the level of acrolein after ICH in mouse brain.In primary neurons,acrolein induced an increase in mitochondrial fragmentation,loss of mitochondrial membrane potential,generation of reactive oxidative species,and release of mitochondrial cytochrome c.Mechanistically,acrolein facilitated the translocation of dynaminrelated protein 1(Drpl)from the cytoplasm onto the mitochondrial membrane and led to excessive mitochondrial fission.Further studies found that treatment with hydralazine(an acrolein scavenger)significantly reversed Drpl translocation and the morphological damage of mitochondria after ICH.In parallel,the neural apoptosis,brain edema,and neurological functional deficits induced by ICH were also remarkably alleviated.In conclusion,our results identify acrolein as an important contributor to the secondary brain injury following ICH.Meanwhile,we uncovered a novel mechanism by which Drpl-mediated mitochondrial oxidative damage is involved in acroleininduced brain injury. | Xun Wu Wenxing Cui Wei Guo Haixiao Liu Jianing Luo Lei Zhao Hao Guo Longlong Zheng Hao Bai Dayun Feng Yan Qu | 2020 | Neuroscience Bulletin2020，36，10： | 3 |
| 4 | 肼苯哒嗪减轻创伤性脑损伤后的认知功能障碍显示文摘目的探讨丙烯醛(Acr)清除剂肼苯哒嗪(Hyd)对创伤性脑损伤(TBI)后认知功能障碍的治疗作用及其可能机制。方法先将成年(6~8周)C57BL/6雄性小鼠随机分为假手术组(Sham组)和TBI后不同时间点(术后3、7、14、28 d)4个亚组,通过Western blotting检测海马区Acr水平的变化情况,然后再将小鼠随机分为Sham组、TBI组和TBI+Hyd(Acr清除剂)干预组,分别通过Morris水迷宫实验、Western blotting以及ELISA检测技术等评估各组小鼠的认知功能、神经突触蛋白的表达量以及线粒体生物发生等变化。结果与Sham组相比,TBI后小鼠海马区Acr水平显著增高。给予Hyd干预能有效减轻小鼠TBI后的认知功能障碍、升高突触相关蛋白的表达水平。并且Hyd治疗明显改善海马区线粒体生物发生和能量代谢,可能是其发挥保护作用的重要机制之一。结论Hyd治疗可促进TBI后海马区线粒体生物发生的恢复,减轻海马神经元的结构与功能损伤,从而改善TBI后的认知功能障碍。 | 吴勋 史英武 屈延 葛顺楠 | 2022 | 空军军医大学学报2022，43，4： | 2 |
| 5 | Acrolein scavenger dimercaprol offers neuroprotection in an animal model of Parkinson’s disease:implication of acrolein and TRPA1显示文摘Background:The mechanisms underlying lesions of dopaminergic(DA)neurons,an essential pathology of Parkinson’s disease(PD),are largely unknown,although oxidative stress is recognized as a key factor.We have previously shown that the pro-oxidative aldehyde acrolein is a critical factor in PD pathology,and that acrolein scavenger hydralazine can reduce the elevated acrolein,mitigate DA neuron death,and alleviate motor deficits in a 6-hydroxydopamine(6-OHDA)rat model.As such,we hypothesize that a structurally distinct acrolein scavenger,dimercaprol(DP),can also offer neuroprotection and behavioral benefits.Methods:DP was used to lower the elevated levels of acrolein in the basal ganglia of 6-OHDA rats.The acrolein levels and related pathologies were measured by immunohistochemistry.Locomotor and behavioral effects of 6-OHDA injections and DP treatment were examined using the open field test and rotarod test.Pain was assessed using mechanical allodynia,cold hypersensitivity,and plantar tests.Finally,the effects of DP were assessed in vitro on SK-N-SH dopaminergic cells exposed to acrolein.Results:DP reduced acrolein and reversed the upregulation of pain-sensing transient receptor potential ankyrin 1(TRPA1)channels in the substantia nigra,striatum,and cortex.DP also mitigated both motor and sensory deficits typical of PD.In addition,DP lowered acrolein and protected DA-like cells in vitro.Acrolein’s ability to upregulate TRPA1 was also verified in vitro using cell lines.Conclusions:These results further elucidated the acrolein-mediated pathogenesis and reinforced the critical role of acrolein in PD while providing strong arguments for anti-acrolein treatments as a novel and feasible strategy to combat neurodegeneration in PD.Considering the extensive involvement of acrolein in various nervous system illnesses and beyond,anti-acrolein strategies may have wide applications and broad impacts on human health. | Liangqin Shi Yazhou Lin Yucheng Jiao Seth AHerr Jonathan Tang Edmond Rogers Zhengli Chen Riyi Shi | 2021 | Translational Neurodegeneration2021，10，2： | 0 |
| 6 | Elevated axonal membrane permeability and its correlation with motor deficits in an animal model of multiple sclerosis显示文摘Background:It is increasingly clear that in addition to myelin disruption,axonal degeneration may also represent a key pathology in multiple sclerosis(MS).Hence,elucidating the mechanisms of axonal degeneration may not only enhance our understanding of the overall MS pathology,but also elucidate additional therapeutic targets.The objective of this study is assess the degree of axonal membrane disruption and its significance in motor deficits in EAE mice.Methods:Experimental Autoimmune Encephalomyelitis was induced in mice by subcutaneous injection of myelin oligodendrocyte glycoprotein/complete Freud’s adjuvant emulsion,followed by two intraperitoneal injections of pertussis toxin.Behavioral assessment was performed using a 5-point scale.Horseradish Peroxidase Exclusion test was used to quantify the disruption of axonal membrane.Polyethylene glycol was prepared as a 30%(w/v)solution in phosphate buffered saline and injected intraperitoneally.Results:We have found evidence of axonal membrane disruption in EAE mice when symptoms peak and to a lesser degree,in the pre-symptomatic stage of EAE mice.Furthermore,polyethylene glycol(PEG),a known membrane fusogen,significantly reduces axonal membrane disruption in EAE mice.Such PEG-mediated membrane repair was accompanied by significant amelioration of behavioral deficits,including a delay in the emergence of motor deficits,a delay of the emergence of peak symptom,and a reduction in the severity of peak symptom.Conclusions:The current study is the first indication that axonal membrane disruption may be an important part of the pathology in EAE mice and may underlies behavioral deficits.Our study also presents the initial observation that PEG may be a therapeutic agent that can repair axolemma,arrest axonal degeneration and reduce motor deficits in EAE mice. | Gary Leung Melissa Tully Jonathan Tang Shengxi Wu Riyi Shi | 2017 | Translational Neurodegeneration2017，6，1： | 0 |
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