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2020, 37(12):1239-1243.doi:10.13213/j.cnki.jeom.2020.20355

纳米氧化铈和炎症关系的研究进展


内蒙古科技大学包头医学院基础医学与法医学院, 内蒙古 包头市 014040

收稿日期: 2020-07-19;  录用日期:2020-10-21;  发布日期: 2021-01-06

基金项目: 国家自然科学基金地区基金项目(81860584)

通信作者: 刘扬, Email: liuyang_bt@163.com  

作者简介: 赵金慧(1994-), 女, 硕士生, 初级检验师; E-mail:1403650465@qq.com

利益冲突  无申报

纳米氧化铈(CeO2NPs)是一种广泛应用的纳米稀土金属氧化物。实验研究证明,CeO2NPs具有类似于超氧化物歧化酶和过氧化氢酶的抗氧化活性,有助于缓解或减轻炎症反应,具有抗炎作用。同时,CeO2NPs能通过氧化应激反应诱导细胞毒性,具有致炎作用。本文归纳总结了CeO2NPs在不同浓度、摄入途径和粒径下与炎症的关系:CeO2NPs在机体聚集的浓度越大越容易表现出致炎作用,不同摄入途径在体内聚集的部位不同,而CeO2NPs粒径越小越容易表现出抗炎作用。

关键词: 纳米氧化铈;  炎症;  浓度;  摄入途径;  粒径 

纳米粒子通常被定义为至少有一维 < 100 nm的粒子,具有独特的物理化学性质[1]。纳米氧化铈(CeO2NPs)因其独特的理化性质在工业领域被用作燃料添加剂、电材材料、气体传感器,并且在生物医学领域也有广泛应用。CeO2NPs在治疗癌症[2]、肥胖[3]、阿尔茨海默病[4]等疾病方面已取得一定进展。研究发现CeO2NPs具有抗炎作用[5-6],但也会诱导炎症发生。CeO2NPs的抗炎作用主要是依靠其强大的抗氧化作用[7],作为一种可再生的抗氧化剂,CeO2NPs具有类似于超氧化物歧化酶和过氧化氢酶的活性,可以通过清除体内自由基[8],减少氧化应激反应,进而减弱氧化应激介导的炎症作用[9]。而CeO2NPs的致炎作用主要与其诱导的氧化应激有关,主要表现为降低机体抗氧化物质水平以及活性氧(reactive oxygen species,ROS)的产生。CeO2NPs通过降低体内的抗氧化剂水平使自由基增多,导致机体抗氧化系统紊乱,进而引起氧化应激反应[10],诱导炎症发生。研究证明CeO2NPs诱导ROS生成会造成细胞毒性,促使细胞DNA损伤和凋亡[11],同时ROS可以诱导炎症因子产生,通过激活参与炎症反应的丝裂原活化蛋白激酶通路引发炎症反应[12-13]

CeO2NPs这种看似矛盾的性能,归因于其独特的空间结构。CeO2晶体具有萤石立方结构,其中八面体空隙为Ce4+,四面体空隙为O2-。缺氧条件下晶体表面形成氧空位,Ce4+转变为Ce3+,ROS存在条件下氧空位消除,Ce3+转变为Ce4+。Ce3+和Ce4+之间相互转换,使CeO2NPs具有抗氧化和促氧化作用[14],抗氧化作用保护细胞免受辐射损伤、氧化应激和炎症的损害;而促氧化作用会诱导氧化应激反应,表现出对细胞的毒性,虽有抗菌作用但也会损伤正常细胞[15]。CeO2NPs中会同时存在Ce3+和Ce4+,但当粒径减小时其表面形成的氧空位增多,所以Ce3+浓度随着CeO2NPs粒径减小而增加[16-17],CeO2NPs表现出抗炎作用。另外CeO2NPs在体内聚集达到一定浓度时会对机体产生毒性作用,诱导炎症发生[18],而且不同给药方式也会影响CeO2NPs在体内的作用[8]。所以确定合适的粒径、浓度以及摄入途径是CeO2NPs表现出抗炎或致炎作用的关键。本文从浓度、摄入途径以及粒径三个方面描述CeO2NPs与炎症的关系,为今后开展相关研究提供依据。

1   CeO2NPs与炎症的关系

1.1   浓度

在确定粒径和摄入途径的前提下,CeO2NPs浓度的大小直接影响其在机体内发挥的是抗炎还是致炎作用。Oró等[19]对大鼠连续2周静脉注射粒径为4~20 nm、0.1 mg·kg-1的CeO2NPs后发现,CeO2NPs可减弱炎症细胞因子表达,使肝损伤标记物丙氨酸转氨酶、天冬氨酸转氨酶水平降低。此外CeO2NPs还可以通过降低一氧化氮和髓过氧化物酶水平减弱炎症反应[20]。给大鼠一次性静脉注射85 mg·kg-1 CeO2NPs(5 nm粒径范围内)后发现,CeO2NPs会在肝内蓄积且难以清除,通过降低过氧化氢酶和抗氧化标志物谷胱甘肽过氧化物酶水平,诱导氧化应激,引发慢性炎症,同时也会导致急性和亚急性肝损伤[21]

浓度对CeO2NPs的影响在细胞中表现得更加突出。将粒径 < 80 nm、质量浓度分别为20 mg·L-1和50 mg·L-1的CeO2NPs与神经元样PC12细胞共同孵育72 h,发现CeO2NPs可以清除PC12细胞中的ROS,下调细胞中参与炎症过程的基因表达,减少炎症发生[22]。CeO2NPs的抗氧化作用可以减少细胞膜和蛋白质的氧化损伤,抑制巨噬细胞产生一氧化氮和炎性细胞因子,并增强炎症细胞的吞噬能力,抑制炎症发生[23-24]。将上皮结肠腺癌细胞(Caco-2细胞)暴露于粒径 < 25 nm、0.001 μmol·L-1(172 mg·L-1)的CeO2NPs中仅2 h后发现,CeO2NPs进入细胞后便导致细胞器功能受损,线粒体内空泡增多,脂肪颗粒增加,核色素沉着[25]。CeO2NPs对细胞的毒性作用主要是因为ROS诱导氧化应激[11],同时这也是导致炎症发生的主要原因之一。ROS可以通过激活炎症信号通路,使一些炎症细胞因子的转录活性增加,进而引起炎症反应[26]

CeO2NPs究竟是发挥抗炎还是致炎作用,与其在机体的沉积浓度密切相关。CeO2NPs主要通过尿液和粪便清除[27]。但若进入体内的CeO2NPs超过机体清除能力便会沉积在细胞组织中,引发毒性作用,所以相同条件下高剂量(每kg体重几十至几百mg)的CeO2NPs往往更容易引发炎症反应[28-29],而且高浓度的CeO2NPs容易聚集成团,更易引起毒性作用[30-31]。相对而言,较低浓度(每kg体重十分之几mg或μg)的CeO2NPs通常不会诱导炎症发生,在摄入途径和给药方式相同时,在此浓度下的CeO2NPs不论是一次性还是连续2周持续给药,都有抗炎作用[19, 32],可能是因为CeO2NPs进入机体发挥作用后能够被及时清除,没有在组织沉积。

1.2   摄入途径

经口一次性摄入粒径在5~20 nm、1 mg·kg-1的CeO2NPs能有效降低应激性胃溃疡大鼠血清中炎症细胞因子白介素(interleukin,IL)-1β水平,减轻胃黏膜炎症[33]。减轻炎症的机制之一可能是CeO2NPs的抗氧化性[34]。CeO2NPs能调节与抗氧化应激有关的核因子-κΒ和核转录因子红系2相关因子2通路,减少ROS和炎症细胞因子如肿瘤坏死因子-α、IL-6、IL-1β的产生,发挥抗炎作用[9, 35]。而另有研究者发现,采用气管滴注的方式给大鼠一次性滴入平均粒径20nm、1mg·kg-1的CeO2NPs后发现,CeO2NPs可以导致肺部炎症,表现为肺泡巨噬细胞数量和体积增加,以及白细胞持续浸润肺泡腔[32]。炎症的发生与CeO2NPs诱导的氧化应激密切相关,而且CeO2NPs能够激活与炎症相关的M1型肺泡巨噬细胞表达,分泌大量炎症细胞因子IL-12,诱导炎症发生[36]。给大鼠单次静脉注射和单次口服粒径 < 20 nm、300 mg·kg-1的CeO2NPs 24 h后发现,通过静脉摄入的CeO2NPs极易沉积在组织中,且导致肝脏出现空泡化等不良反应,而经口摄入的CeO2NPs短时间内在组织中并没有沉积,主要通过粪便排出体外,一过性的CeO2NPs并未造成组织细胞损伤[37]

由此可知,不同途径摄入的CeO2NPs在体内聚集的部位和浓度不同。相同条件下通过静脉摄入比经口摄入更容易沉积在组织中,且通过静脉摄入时,肝脏和脾脏损伤最明显[37];通过呼吸道进入体内的CeO2NPs更容易引发肺部炎症[38],并且存在于肺组织的纳米粒子会穿透肺泡壁进入全身循环。CeO2NPs的低溶解度使其在器官持续存在并且在肝、肾、脾和血液中累积,引发炎症反应[39-41]。不仅如此,CeO2NPs还可通过嗅觉传导通路导致神经元损伤[42]。研究表明吸入CeO2NPs后,动脉粥样硬化易感小鼠小脑和脑干中炎症细胞因子、肿瘤坏死因子水平升高[43]

1.3   粒径

通常在粒径较小的情况下,CeO2NPs更容易表现出抗炎作用。Golyshkin等[33]认为CeO2NPs应用于生物医学领域时,粒径在3~7 nm时是最安全的。粒径大于100 nm的氧化铈颗粒具有弱毒性,粒径在50~100 nm之间的CeO2NPs能够引起氧化应激反应,诱导炎症发生[44]。CeO2NPs进入机体前后的粒径会有所不同。粒径在18~150 nm的CeO2NPs进入组织后会聚集成团,形成较大颗粒,有的粒径甚至高达670 nm[36, 45]。需要注意的是,粒径的大小虽然影响CeO2NPs对机体的作用,但并不是起决定性作用。在胃溃疡大鼠模型中,经口一次摄入1 mg·kg-1、粒径分别为5 nm和160 nm的CeO2NPs后发现,两种粒径下CeO2NPs均可通过减弱氧化应激反应,抑制溃疡发生[33, 46]。此外研究还发现吸入的纳米颗粒在嗅觉区域的沉积量和粒径有关,在粒径为1~100 nm的纳米粒子中,粒径为5 nm左右的纳米粒子的沉积量最高[42]

不同粒径下CeO2NPs表现的Ce4+和Ce3+比例不同。随着粒径的减小,CeO2NPs更容易表现为Ce3+,而粒径增大时Ce4+增多[16]。CeO2NPs表现出Ce3+时能有效清除羟基自由基[47],清除能力随着Ce3+浓度增加而增强[48]。当浓度一定时,粒径在7.1~14.7 nm比粒径更小的CeO2NPs能够清除更多的自由基,因为极小粒径下的CeO2NPs容易发生团聚,表面积减小的同时CeO2NPs对羟自由基清除能力减弱[49]。而当CeO2NPs过多表现出Ce4+时容易产生促氧化作用[14, 50],这可能会诱导ROS产生,对组织细胞产生氧化应激作用,导致炎症发生。

2   总结

本文从浓度、摄入途径以及粒径三个方面描述了CeO2NPs与炎症的关系。CeO2NPs对细胞、组织器官甚至全身炎症都有显著的抗炎作用,不论是单独用药还是和其他药物联用抗炎,都使其有望成为21世纪治疗炎症相关疾病的有效药物之一。但与此同时它的致炎作用也不容忽视。使CeO2NPs导致炎症作用的根本原因是纳米颗粒在组织细胞中的聚集量。不同摄入途径影响CeO2NPs在组织聚集的部位,导致局部浓度过高,最终引发炎症反应。而当CeO2NPs浓度增大时,更容易聚集形成更大的颗粒,通常会表现出致炎作用。目前虽已有很多研究表明CeO2NPs具有抗炎或致炎作用,但在不同浓度、摄入途径以及粒径影响下,寻求CeO2NPs安全有效无毒的作用方式,这将是以后需要共同关注研究的重点。不论是工业领域还是医学领域应用,都要保证CeO2NPs在不造成机体损伤情况下发挥其性能。

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[基金项目] 国家自然科学基金地区基金项目(81860584)

[作者简介]

[收稿日期] 2020-07-19

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纳米氧化铈和炎症关系的研究进展

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