Formaldehyde-induced hematopoietic stem and progenitor cell toxicity in mouse lung and nose
作者：
Zhao, Yun;Magana, Laura C.;Cui, Haiyan;Huang, Jiawei;McHale, Cliona M.;...
期刊：
Archives of Toxicology ,2021年95(2):693-701 ISSN：0340-5761
通讯作者：
Zhang, Luoping;Li, Rui
作者机构：
[Zhang, Luoping; McHale, Cliona M.; Zhao, Yun; Magana, Laura C.] Univ Calif Berkeley, Sch Publ Hlth, Div Environm Hlth Sci, Berkeley, CA 94720 USA.;[Li, Rui; Yang, Xu; Zhao, Yun; Huang, Jiawei; Cui, Haiyan] Cent China Normal Univ, Sch Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan, Peoples R China.;[Looney, Mark R.] Univ Calif San Francisco UCSF, Dept Med, San Francisco, CA USA.;[Looney, Mark R.] Univ Calif San Francisco UCSF, Dept Lab Med, San Francisco, CA USA.
通讯机构：
[Zhang, Luoping] U;[Li, Rui] C;Univ Calif Berkeley, Sch Publ Hlth, Div Environm Hlth Sci, Berkeley, CA 94720 USA.;Cent China Normal Univ, Sch Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan, Peoples R China.
关键词：
Colony;Formaldehyde;HSC/HPC;Leukemogenesis;Toxicity
摘要：
Formaldehyde (FA), an economically important and ubiquitous chemical, has been classified as a human carcinogen and myeloid leukemogen. However, the underlying mechanisms of leukemogenesis remain unclear. Unlike many classical leukemogens that damage hematopoietic stem/progenitor cells (HSC/HPC) directly in the bone marrow, FA—as the smallest, most reactive aldehyde—is thought to be incapable of reaching the bone marrow through inhalation exposure. A recent breakthrough study discovered that mouse lung contains functional HSC/HPC that can produce blood cells and travel bi-directionally between the lung and bone marrow, while another early study reported the presence of HSC/HPC in rat nose. Based on these findings, we hypothesized that FA inhalation could induce toxicity in HSC/HPC present in mouse lung and/or nose rather than in the bone marrow. To test this hypothesis, we adapted a commercially available protocol for culturing burst-forming unit-erythroid (BFU-E) and colony-forming unit-granulocyte, macrophage (CFU-GM) colonies from bone marrow and spleen to also enable culture of these colonies from mouse lung and nose, a novel application of this assay. We reported that in vivo exposure to FA at 3mg/m3 or ex vivo exposure up to 400µM FA decreased the formation of both colony types from mouse lung and nose as well as from bone marrow and spleen. These findings, to the best of our knowledge, are the first empiricallyto show that FA exposure can damage mouse pulmonary and olfactory HSC/HPC and provide potential biological plausibility for the induction of leukemia at the sites of entry rather than the bone marrow. © 2020, Springer-Verlag GmbH Germany, part of Springer Nature.
语种：
英文
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低浓度甲醛和PM_(2.5)联合暴露对哮喘小鼠的影响
作者：
鲁娴娴;黄佳伟;崔海燕;吕柯;赵元腾;...
期刊：
中国环境科学 ,2020年40(3):1335-1344 ISSN：1000-6923
作者机构：
华中师范大学生命科学学院遗传调控与整合生物学湖北省重点实验室,湖北 武汉 430079
关键词：
低浓度;甲醛;联合暴露;哮喘
摘要：
为探究低浓度甲醛(FA)单独及与PM_(2.5)联合暴露对哮喘小鼠的影响,选取70只雄性Balb/c小鼠,随机分为5组,分别为:对照组、卵清蛋白(OVA)组、FA+OVA组、PM_(2.5)+OVA组、FA+PM_(2.5)+OVA组,每组14只,其中6只进行气道高反应性(AHR)检测,其余8只用于检测血清T-IgE、肺泡灌洗液(BALF)中IFN-γ、IL-4以及肺组织中活性氧(ROS)、丙二醛(MDA)的含量,并对BALF中炎症细胞进行计数.同时对小鼠肺组织进行H&E染色以及p-p38MAPK和p-p65NF-kB免疫组化分析.结果显示,与OVA组相比,0.5mg/m~3FA单独暴露组哮喘小鼠肺部MDA水平显著升高(P<0.001),肺部炎症细胞呈现上升趋势(P>0.05),0.5mg/m~3FA和0.5mg/kg PM_(2.5)联合暴露组哮喘小鼠肺部炎症显著加重(P<0.05或P<0.01),肺功能减弱(P<0.01),肺部氧化应激水平以及p38MAPK和NF-kB的磷酸化水平均显著升高(P<0.05或P<0.001),Th2型细胞因子释放显著增加(P<0.01).因此,低浓度FA单独暴露会加重哮喘小鼠肺部损伤而非抑制,并且可进一步促进PM_(2.5)对哮喘小鼠肺部的损伤,即低浓度FA和PM_(2.5)联合暴露会对哮喘小鼠肺部造成严重损害,这可能与ROS介导的p38MAPK途径加剧Thl/Th2型免疫反应失衡有关.
语种：
中文
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Validation of an in vivo electrochemical immunosensing platform for simultaneous detection of multiple cytokines in Parkinson’s disease mice model
作者：
Shen, Zhuping;Huang, Jiawei;Wei, Hui;Niu, Huan;Li, Bitong;...
期刊：
Bioelectrochemistry ,2020年134:107532 ISSN：1567-5394
通讯作者：
Liu, Guozhen
作者机构：
[Shen, Zhuping; Liu, Guozhen; Wei, Hui] Cent China Normal Univ, Int Joint Res Ctr Intelligent Biosensor Technol &, Wuhan 430079, Peoples R China.;[Li, Rui; Huang, Jiawei] Cent China Normal Univ, Sch Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan 430079, Peoples R China.;[Niu, Huan; Li, Bitong; Liu, Guozhen] Univ New South Wales, Fac Engn, Grad Sch Biomed Engn, Sydney, NSW 2052, Australia.;[Liu, Guozhen] Univ New South Wales, Australian Ctr NanoMed, Sydney, NSW 2052, Australia.;[Liu, Guozhen] Univ New South Wales, Grad Sch Biomed Engn, Sydney, NSW, Australia.
通讯机构：
[Liu, Guozhen] U;Univ New South Wales, Grad Sch Biomed Engn, Sydney, NSW, Australia.
关键词：
Cytokines;Electrochemical immunosensors;Multiplex sensing;In vivo detection;Parkinson's disease;Mouse brain
摘要：
Parkinson's Disease (PD) is a neurodegenerative chronic disorder which destroys brain tissue and result in impaired movement. Early diagnosis of PD before the appearance of clinical symptom is vital for effective treatment. High levels of proinflammatory cytokines found in PD patient's brains, as natural inflammation response product, are potential biomarkers for PD detection in the early stage. Herein, we developed an in vivo electrochemical immunosensing device based on glassy carbon rod to simultaneously detect three proinflammatory cytokines (IL-1β, IL-6 and TNF-α). The levels of IL-1β, IL-6 and TNF-α secreted by N2a cells significantly increased within 24 h after lipopolysaccharide (LPS) stimulation. Under in vivo conditions, the concentrations of IL-1β, IL-6 and TNF-α in PD model group achieved by injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) intraperitoneally, were significantly higher than those in the control mouse group. The concentrations of three cytokines in vivo/vitro detected by this immunosensing device was comparable to that obtained by ELISA. Furthermore, this deployable immunosensing device was proved to be highly sensitive with the limits of detection (LODs) of 5 pg mL−1 for each cytokine, specific and reliable, suggesting its potential to be a universal immunosensing platform for early identification and diagnosis of PD in vivo in the future. © 2020 Elsevier B.V.
语种：
英文
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Combined exposure to formaldehyde and PM2.5: Hematopoietic toxicity and molecular mechanism in mice
作者：
Ge, Jing;Yang, Honglian;Lu, Xianxian;Wang, Shenqi;Zhao, Yun;...
期刊：
Environment International ,2020年144:106050 ISSN：0160-4120
通讯作者：
Li, Rui;Zhang, Luoping
作者机构：
[Li, Rui; Zhao, Yun; Huang, Jiawei; Lu, Xianxian; Ge, Jing] Cent China Normal Univ, Sch Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan 430079, Peoples R China.;[Zhang, Luoping] Univ Calif Berkeley, Sch Publ Hlth, Div Environm Hlth Sci, Berkeley, CA 94720 USA.;[Xi, Zhuge; Yang, Honglian] Tianjin Inst Environm & Operat Med, Tianjin 300050, Peoples R China.;[Wang, Shenqi; Ge, Jing] Huazhong Univ Sci & Technol, Coll Life Sci & Technol, Wuhan 430074, Peoples R China.
通讯机构：
[Li, Rui] C;[Zhang, Luoping] U;Cent China Normal Univ, Sch Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan 430079, Peoples R China.;Univ Calif Berkeley, Sch Publ Hlth, Div Environm Hlth Sci, Berkeley, CA 94720 USA.
关键词：
PM2.5;Formaldehyde;Combined exposure;Hematopoietic toxicity;Molecular mechanism
摘要：
PM2.5 and formaldehyde (FA) are major outdoor and indoor air pollutants in China, respectively, and both are known to be harmful to human health and to be carcinogenic. Of all the known chronic health effects, leukaemia is one of the most serious health risks associated with these two pollutants. To explore the influence and underlying mechanisms of exposure to formaldehyde and PM2.5 on hematopoietic toxicity, we systematically studied the toxicity induced in hematopoietic organs: bone marrow (BM); spleen; and myeloid progenitor cells (MPCs). Male Balb/c mice were exposed to: PM2.5 (20, 160 μg/kg·d) at a dose of 40 μL per mouse or formaldehyde (0.5, 3.0 mg/m3) for 8 h per day for 2 weeks or co-exposed to formaldehyde and PM2.5 (20 μg/kg·d PM2.5 + 0.5 mg/m3 FA, 20 μg/kg·d PM2.5 + 3 mg/m3 FA, 160 μg/kg·d PM2.5 + 0.5 mg/m3 FA, 160 μg/kg·d PM2.5 + 3 mg/m3 FA) for 2 weeks. Similar toxic effects were found in the formaldehyde-only and PM2.5-only groups, including significant decrease of blood cells and MPCs, along with decreased expression of hematopoietic growth factors. In addition, individual exposure of formaldehyde or PM2.5 increased oxidative stress, DNA damage and immune system disorder by destroying the balance of Th1/Th2, and Treg/Th17. DNA repair was markedly inhibited by deregulating the mammalian target of rapamycin (mTOR) pathway. Combined exposure to PM2.5 and formaldehyde led to more severe effects. Administration of Vitamin E (VE) was shown to attenuate these effects. In conclusion, our findings suggested that PM2.5 and formaldehyde may induce hematopoietic toxicity by reducing the expression of hematopoietic growth factors, increasing oxidative stress and DNA damage, activating the ‘immune imbalance’ pathway and suppressing the DNA-repair related mTOR pathway. The hematopoietic toxicity induced by combined exposure of PM2.5 and formaldehyde might provide further insights into the increased incidence of hematological diseases, including human myeloid leukaemia. © 2020 The Authors
语种：
英文
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除草剂三氟羧草醚经口暴露对小鼠学习记忆能力的影响
作者：
张倩;杜俊停;黄佳伟;崔海燕;路曼曼;...
期刊：
环境科学学报 ,2019年39(2):633-639 ISSN：0253-2468
通讯作者：
Yuan, J.
作者机构：
华中师范大学生命科学学院,遗传调控与整合生物学湖北省重点实验室,武汉430079;[路曼曼; 黄佳伟; 袁均林; 陈明清; 李睿; 张倩; 丁书茂; 杜俊停; 崔海燕] 华中师范大学
通讯机构：
Hubei Key Laboratory of Genetic Regulation and Integrative Biology, College of Life Science, Central China Normal University, Wuhan, China
关键词：
三氟羧草醚;学习记忆;氧化应激
摘要：
目前,有关三氟羧草醚( Acifluorfen,AF)的神经毒性未见报道且亟待确定.为探讨AF经口暴露对小鼠学习记忆能力的影响及其可能机制,将30只雄性昆明小鼠随机分成生理盐水对照组、0.13、1.3、13和130 mg·kg~(-1)·d~(-1) AF染毒组共5组,灌胃染毒14 d,进行Morris水迷宫实验,观察脑海马病理切片,并检测脑组织中活性氧( ROS) 、丙二醛( MDA) 、还原型谷胱甘肽( GSH) 、磷酸化cAMP反应元件结合蛋白( pCREB)和脑源性神经营养因子( BDNF)含量.结果显示,与对照组相比,AF染毒剂量分别为13和130 mg·kg~(-1)·d~(-1)时,小鼠行为学上学习记忆能力下降;海马细胞排列松散;出现氧化损伤,其中,ROS含量显著升高( p<0.05) ,GSH含量显著减少( p<0.05) ;神经保护能力减弱,其中,pCREB和BDNF水平显著( p<0.05)或极显著( p<0.01)下降.结果表明,AF能够导致小鼠学习记忆能力下降,氧化应激和CREB-BDNF通路级联下调可能是AF造成神经毒性的机制之一.
语种：
中文
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Antagonistic effect of epigallocatechin-3-gallate on neurotoxicity induced by formaldehyde
作者：
Huang, Jiawei;Lu, Yu;Zhang, Bin;Yang, Shaoping;Zhang, Qian;...
期刊：
Toxicology ,2019年412:29-36 ISSN：0300-483X
通讯作者：
Li, Rui
作者机构：
[Cuia, Haiyan; Li, Rui; Yang, Xu; Zhang, Qian; Zhao, Yun; Huang, Jiawei; Lu, Xianxian; Lu, Yu] Cent China Normal Univ, Sch Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan 430079, Hubei, Peoples R China.;[Zhang, Bin; Yang, Shaoping] Huazhong Univ Sci & Technol, Wuhan Childrens Hosp, Tongji Med Coll, Wuhan 430016, Hubei, Peoples R China.
通讯机构：
[Li, Rui] C;Cent China Normal Univ, Sch Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan 430079, Hubei, Peoples R China.
关键词：
*EGCG;*Formaldehyde;*Neurotoxicity;*Nrf2;*Oxidative stress
摘要：
The toxicity of formaldehyde (FA) has always been of great concern, particularly since its use is unavoidable. On the other hand, epigallocatechin-3-gallate (EGCG), an active substance in tea polyphenols, has been shown to demonstrate physiological protective functions by in both epidemiological and zoological studies, particularly in the nervous system. The study described here, aims to explore whether EGCG can alleviate the neurotoxic effects induced by formaldehyde. After 14 days of exposure to 3 mg/m(3) formaldehyde, mice exhibited significant cognitive impairment. In the FA group, a significant increase in iNOS level compared with the control group was observed. The reduced GSH level was significantly decreased. The levels of IL-1beta, TNF-alpha and Caspase-3 were obviously raised, while H&E and Nissl staining illustrated significant neuronal damage. After administering EGCG as a protective agent, all the above observed changes were reversed, and the protective effect of EGCG became gradually evident in the 20-500 mg/kg range. Immunohistochemistry results showed that EGCG could activate the Nrf2 signaling pathway, thus alleviating the oxidative damage caused by formaldehyde.
语种：
英文
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Antagonistic effect of vitamin E on nAl2O3-induced exacerbation of Th2 and Th17-mediated allergic asthma via oxidative stress
作者：
Cui, Haiyan;Huang, Jiawei;Lu, Manman;Zhang, Qian;Qin, Wei;...
期刊：
Environmental Pollution ,2019年252(Pt B):1519-1531 ISSN：0269-7491
通讯作者：
Li, Rui
作者机构：
[Lu, Manman; Li, Rui; Zhang, Qian; Zhao, Yun; Huang, Jiawei; Lu, Xianxian; Cui, Haiyan; Qin, Wei] Cent China Normal Univ, Hubei Key Lab Genet Regulat & Integrat Biol, Sch Life Sci, Wuhan 430079, Hubei, Peoples R China.;[Zhang, Jiting] Cent China Normal Univ, Inst Nanosci & Nanotechnol, Coll Phys Sci & Technol, Wuhan 430079, Hubei, Peoples R China.;[Xi, Zhuge] Tianjin Inst Environm & Operat Med, 1 Dali Rd, Tianjin 300050, Peoples R China.
通讯机构：
[Li, Rui] C;Cent China Normal Univ, Hubei Key Lab Genet Regulat & Integrat Biol, Sch Life Sci, Wuhan 430079, Hubei, Peoples R China.
关键词：
Aluminum oxide nanopowder;Allergic asthma;Oxidative stress;Th2/Th17;Vitamin E
摘要：
Some basic research has shown that nanomaterials can aggravate allergic asthma. However, its potential mechanism is insufficient. Based on the research that alumina nanopowder (nAl2O3) has been reported to cause lung tissue damage, the purpose of this study was to explore the relationship between nAl2O3 and allergic asthma as well as its molecular mechanism. In this study, Balb/c mice were sensitized with ovalbumin (OVA) to construct the allergic asthma model while intratracheally administered 0.5, 5 or 50 mg kg−1·day−1 nAl2O3 for 3 weeks. It was observed that exposure to nAl2O3 exacerbated airway hyperresponsiveness (AHR), airway remodeling, and inflammation cell infiltration, leading to lung function damage in mice. Results revealed that nAl2O3 could increase ROS levels and decrease GSH levels in lung tissue, promote the increases of the T-IgE, TGF-β, IL-1β and IL-6 levels, stimulate the overexpression of transcription factors GATA-3 and RORγt, decrease the levels of IFN-γ and IL-10 and increase the levels of IL-4 and IL-17A, resulting in the imbalance of Th1/Th2 and Treg/Th17 immune responses. In addition, antioxidant Vitamin E (Vit E) could alleviate asthma-like symptoms through blocking oxidative stress. The study displayed that exposure of nAl2O3 deteriorated allergic asthma through promoting the imbalances of Th1/Th2 and Treg/Th17. Main finding: Intratracheal instillation of nAl2O3 aggravated the imbalance of th2-type th17-type immune, induced airway hyperresponsiveness and subsequently deteriorated allergic asthma in mice. © 2019
语种：
英文
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PM_(2.5)通过NF-κB/NLRP3途径促进金黄色葡萄球菌肺炎的研究
作者：
黄佳伟;鲁娴娴;崔海燕;张斌;陈鹏;...
期刊：
生态毒理学报 ,2019年14(5):133-143 ISSN：1673-5897
作者机构：
华中师范大学生命科学学院,武汉 430079;华中科技大学同济医学院附属武汉儿童医院,武汉 430016;[黄佳伟; 杨旭; 李睿; 鲁娴娴; 崔海燕] 华中师范大学;[杨少萍; 陈鹏; 张斌] 武汉市儿童医院
关键词：
金黄色葡萄球菌肺炎;小鼠;氧化应激
摘要：
细颗粒物(PM_(2.5))引发的呼吸系统疾病近年来成为公众关注焦点。为探究PM_(2.5)在金黄色葡萄球菌肺炎中产生的效应及其相关分子机制,将Balb/c小鼠随机分成6组:A.生理盐水对照,B.5 mg·kg~(-1) PM_(2.5),C.肺炎模型,D.肺炎模型+0.05 mg·kg~(-1) PM_(2.5),E.肺炎模型+0.5 mg·kg~(-1) PM_(2.5),F.肺炎模型+5 mg·kg~(-1) PM_(2.5),进行为期7 d的PM_(2.5)气道滴注暴露后,用细菌滴鼻构建金黄色葡萄球菌肺炎模型。结果发现,PM_(2.5)暴露造成了小鼠肺部损伤并促进了金黄色葡萄球菌肺炎,并随着PM_(2.5)浓度的升高愈发显著,体现为小鼠肺部出现了更显著的气道重塑、炎症细胞浸润现象,肺纤维化程度加深。其分子机制是PM_(2.5)首先引发小鼠肺部产生氧化应激,促进核因子κB(NF-κB)信号通路的激活,进而介导炎症小体NLRP3的活化,导致白细胞介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)表达升高,最终恶化了金黄色葡萄球菌肺炎。
语种：
中文
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纳米Al_2 O_3经气道滴注致小鼠脏器损伤和炎症反应的研究
作者：
崔海燕;李丹;王吉燕;路曼曼;黄佳伟;...
期刊：
环境科学学报 ,2019年39(3):969-977 ISSN：0253-2468
通讯作者：
Li, R.
作者机构：
华中师范大学生命科学学院,遗传调控与整合生物学湖北省重点实验室,武汉430079
通讯机构：
Key Laboratory of Genetic Regulation and Integrated Biology of Hubei Province, School of Life Sciences, Central China Normal University, Wuhan, China
关键词：
纳米氧化铝（nAl2O3）;脏器;氧化应激;炎症反应;维生素E
摘要：
为探讨纳米氧化铝(nAl_2O_3)气道滴注对小鼠脏器的毒性作用,本研究将Balb /c小鼠随机分成6组:生理盐水组、50 mg·kg~(-1)·d~(-1) Vit E(维生素E)组、0.5 mg·kg~(-1)·d~(-1) nAl_2O_3组、5 mg·kg~(-1)·d~(-1) nAl_2O_3组、50 mg·kg~(-1)·d~(-1) nAl_2O_3组、nAl_2O_3 50+Vit E组(50 mg·kg~(-1)·d~(-1) nAl_2O_3 +50 mg·kg~(-1)·d~(-1)Vit E) .实验周期为21 d,气道滴注暴露,隔天滴注,维生素E灌胃阻断.染毒结束后,检测肺部、脾脏、肝脏和肾脏中活性氧(Reactive Oxide Species,ROS)和还原型谷胱甘肽(Glutathione,GSH)含量,并进行肺部病理学观察和肺泡灌洗液细胞计数.结果表明:与对照组相比, nAl_2O_3剂量为0.5 mg·kg~(-1)·d~(-1)时,小鼠肺部ROS含量增加(p<0.05) ,肝脏GSH含量下降(p<0.05) ; nAl_2O_3剂量为5和50 mg·kg~(-1)·d~(-1)时,小鼠肺部、脾脏、肝脏和肾脏ROS含量均显著增加(p<0.05) ,肺部和肝脏GSH含量均显著下降(p<0.05) ;且小鼠肺部出现支气管壁增厚、气道腔皱缩、组织纤维化等气道重塑和嗜酸性粒细胞等炎症细胞浸润现象.而抗氧化剂维生素E的阻断显著降低了肝脏ROS含量,有效恢复了肺部GSH活性(p<0.01) ,且缓解了肺部气道重塑和炎症细胞浸润现象(p<0.05) .研究表明,nAl_2O_3经气道滴注染毒后,不仅会对小鼠肺部造成损伤和炎症反应,同时也能够对脾脏、肝脏和肾脏造成氧化损伤.本研究可为纳米材料的安全性应用及其潜在危害的预防提供科学依据.
语种：
中文
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Vasodilatory effect of formaldehyde via the NO/cGMP pathway and the regulation of expression of KATP, BKCa and L-type Ca(2+) channels.
作者：
Zhao, Yun;Ge, Jing;Li, Xiaoxiao;Guo, Qing;Zhu, Yuqing;...
期刊：
Toxicology Letters ,2019年312:55-64 ISSN：0378-4274
通讯作者：
Yang, Xu;Li, Rui
作者机构：
[Guo, Qing; Yang, X; Li, R; Li, Rui; Li, Xiaoxiao; Yang, Xu; Zhao, Yun; Song, Jing; Ge, Jing; Ding, Shumao] Cent China Normal Univ, Sch Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, 152 Luoyu Rd, Wuhan 430079, Hubei, Peoples R China.;[Zhang, Luoping] Univ Calif Berkeley, Sch Publ Hlth, Div Environm Hlth Sci, Berkeley, CA 94720 USA.;[Guo, Qing] Huazhong Univ Sci & Technol, Sch Publ Hlth, Hangkong Rd, Wuhan 430030, Hubei, Peoples R China.;[Zhu, Yuqing] Zhejiang Univ, Sch Med, Ctr Stem Cell & Regenerat Med, 866 Yuhangtang Rd, Hangzhou 310058, Zhejiang, Peoples R China.
通讯机构：
[Yang, X; Li, R] C;Cent China Normal Univ, Sch Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, 152 Luoyu Rd, Wuhan 430079, Hubei, Peoples R China.
关键词：
Formaldehyde;Ion channels;NO/cGMP pathway;Rat aortas;Vasorelaxation
摘要：
Formaldehyde (FA), a well-known toxic gas molecule similar to nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H2S), is widely produced endogenously via numerous biochemical pathways, and has a number of physiological roles in the biosystem. We attempted to investigate the vasorelaxant effects of FA and their underlying mechanisms. We found that FA induced vasorelaxant effects on rat aortic rings in a concentration-dependent manner. The NO/cyclic guanosine 5' monophosphate (cGMP) pathway was up-regulated when the rat aortas were treated with FA. The expression of large-conductance Ca(2+)-activated K(+) (BKCa) channel subunits alpha and beta of the rat aortas was increased by FA. Similarly, the levels of ATP-sensitive K(+) (KATP) channel subunits Kir6.1 and Kir6.2 were also up-regulated when the rat aortas were incubated with FA. In contrast, levels of the L-type Ca(2+) channel (LTCC) subunits, Cav1.2 and Cav1.3, decreased dramatically with increasing concentrations of FA. We demonstrated that the regulation of FA on vascular contractility may be via the up-regulation of the NO/cGMP pathway and the modulation of ion channels, including the upregulated expression of the KATP and BKCa channels and the inhibited expression of LTCCs. Further study is needed to explore the in-depth mechanisms of FA induced vasorelaxation.
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英文
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New insight into Alzheimer's disease: Light reverses Aβ-obstructed interstitial fluid flow and ameliorates memory decline in APP/PS1 mice
作者：
Xiangpei Yue;Yufei Mei;Yun Zhang;Zheng Tong;Dehua Cui;...
期刊：
Alzheimer's & Dementia: Translational Research & Clinical Interventions ,2019年5(1):671-684 ISSN：2352-8737
通讯作者：
Tong, Z.
作者机构：
[Chunli Duan; Ge Gao; Hui Yang] Department of Neurobiology, School of Basic Medical Sciences, Capital Medical University, Beijing, China;[Dehua Cui; Jun Yang; Aibo Wang; Rui Wang] Department of Radiology, Peking University Third Hospital, Key Laboratory of Magnetic Resonance Imaging Equipment and Technique, Beijing, China;Corresponding author. Tel: +86-010-83950362;Fax: +86-010-83950363.;∗Corresponding author. Tel: 604-822-8019
通讯机构：
[Weihong Song; Hongbin Han] D;[Zhiqian Tong] L;Department of Radiology, Peking University Third Hospital, Key Laboratory of Magnetic Resonance Imaging Equipment and Technique, Beijing, China<&wdkj&>Corresponding author. Tel: +86-010-83950362;Fax: +86-010-83950363.<&wdkj&>∗Corresponding author. Tel: 604-822-8019;Fax: 604-822-7981.<&wdkj&>∗∗Corresponding author. Tel: +86-010-82266972
关键词：
Red light (RL);Alzheimer's disease (AD);Amyloid β (Aβ);Formaldehyde (FA);Formaldehyde dehydrogenase (FDH);Extracellular space (ECS);Interstitial fluid (ISF)
摘要：
Introduction: Pharmacological therapies to treat Alzheimer's disease (AD) targeting "Abeta" have failed for over 100 years. Low levels of laser light can disassemble Abeta. In this study, we investigated the mechanisms that Abeta-blocked extracellular space (ECS) induces memory disorders in APP/PS1 transgenic mice and addressed whether red light (RL) at 630 nm rescues cognitive decline by reducing Abeta-disturbed flow of interstitial fluid (ISF). Methods: We compared the heating effects on the brains of rats illuminated with laser light at 630, 680, and 810 nm for 40 minutes, respectively. Then, a light-emitting diode with red light at 630 nm (LED-RL) was selected to illuminate AD mice. The changes in the structure of ECS in the cortex were examined by fluorescent double labeling. The volumes of ECS and flow speed of ISF were quantified by magnetic resonance imaging. Spatial memory behaviors in mice were evaluated by the Morris water maze. Then, the brains were sampled for biochemical analysis. Results: RL at 630 nm had the least heating effects than other wavelengths associated with ~49% penetration ratio into the brains. For the molecular mechanisms, Abeta could induce formaldehyde (FA) accumulation by inactivating FA dehydrogenase. Unexpectedly, in turn, FA accelerated Abeta deposition in the ECS. However, LED-RL treatment not only directly destroyed Abeta assembly in vitro and in vivo but also activated FA dehydrogenase to degrade FA and attenuated FA-facilitated Abeta aggregation. Subsequently, LED-RL markedly smashed Abeta deposition in the ECS, recovered the flow of ISF, and rescued cognitive functions in AD mice. Discussion: Abeta-obstructed ISF flow is the direct reason for the failure of the developed medicine delivery from superficial into the deep brain in the treatment of AD. The phototherapy of LED-RL improves memory by reducing Abeta-blocked ECS and suggests that it is a promising noninvasive approach to treat AD.
语种：
英文
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Dermal exposure to nano-TiO2 induced cardiovascular toxicity through oxidative stress, inflammation and apoptosis
作者：
Zhang, Qian;Liu, Zhimin;Du, Junting;Qin, Wei;Lu, Manman;...
期刊：
JOURNAL OF TOXICOLOGICAL SCIENCES ,2019年44(1):35-45 ISSN：0388-1350
通讯作者：
Yuan, Junlin
作者机构：
[Lu, Manman; Yuan, Junlin; Liu, Zhimin; Li, Rui; Li, Xiaoxiao; Zhang, Qian; Cui, Haiyan; Du, Junting; Qin, Wei; Ding, Shumao] Cent China Normal Univ, Sch Life Sci, Lab Environm Biomed, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan 430079, Hubei, Peoples R China.
通讯机构：
[Yuan, Junlin] C;Cent China Normal Univ, Sch Life Sci, Lab Environm Biomed, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan 430079, Hubei, Peoples R China.
关键词：
Nano-titanium dioxide (nano-TiO2);Cardiovascular toxicity;Oxidative stress;Inflammation;Cytotoxicity;Apoptosis
摘要：
Due to its excellent properties such as ultraviolet obscuration, chemical stability and small particle size, nano-titanium dioxide (nano-TiO 2 ) is widely used, particularly in sunblock products. The skin is therefore a chief route for exposure. Studies have found that oral or respiratory exposure to nano-TiO 2 has an adverse impact on the cardiovascular system. The relationship between dermal exposure to nano-TiO 2 and cardiovascular system toxicity, particularly the causative mechanisms, remain unclear. In this study, we used Balb/c mice to evaluate cardiovascular toxicity from nano-TiO 2 dermal exposure, and the underlying mechanisms associated with the human umbilical vein endothelial cells (HUVECs) were explored. Our results showed that nano-TiO 2 treatment resulted in an obvious increase in reactive oxygen species and 8-hydroxy-2’-deoxyguanosine, indicating the appearance of oxidative stress. Moreover, the levels of inflammatory biomarkers, such as immunoglobulin E, soluble intercellular adhesion molecule-1, interleukin-8, and hypersensitive C-reactive protein, also increased. Exposing HUVECs to nano-TiO 2 led to a decline in cell vitality, and an increase in caspase-3 levels, suggesting that nano-TiO 2 exposure caused cytotoxicity and even cell apoptosis. Interestingly, neutralizing oxidative stress by administering Vitamin E was shown to reduce the inflammatory response and cytotoxicity. Our findings suggest that nano-TiO 2 can injure the cardiovascular system via dermal exposure, and does this via oxidative stress-induced inflammation and cytotoxicity. Vitamin E treatment may be a strategy to mitigate the damage. © 2019, Japanese Society of Toxicology. All rights reserved.
语种：
英文
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PM2.5经皮肤暴露和气道滴注对小鼠肝脏的不同影响
作者：
路曼曼;宋静;鲁娴娴;张倩;崔海燕;...
期刊：
化学与生物工程 ,2018年35(12):14-19 ISSN：1672-5425
作者机构：
华中师范大学生命科学学院遗传调控与整合生物学湖北省重点实验室,湖北武汉,430079;[路曼曼; 宋静; 李睿; 鲁娴娴; 张倩; 崔海燕] 华中师范大学
关键词：
皮肤暴露;气道滴注;肝脏;氧化应激
摘要：
大气细颗粒物( PM2.5 )可通过呼吸、皮肤接触等途径进入机体,对机体健康产生危害.为了探究 PM2.5 经不同暴露途径对机体产生的不同影响,将小鼠随机分为:对照组,20 μ g·kg^-1 ·d^-1 、100 μ g·kg^-1 ·d^-1 、500 μ g·kg^-1·d^-1 PM2.5 皮肤暴露组和 20 μg·kg^-1 ·d^-1 、100 μ g·kg^-1 ·d^-1 、500 μ g·kg^-1 ·d^-1 PM2.5 气道滴注组.结果表明,随着 PM2.5 浓度的增加,小鼠肝脏细胞空泡化程度增强,同时小鼠肝脏 ROS 、 MDA 、 8 - OHdG 和 ALT 含量升高;PM2.5 经皮肤暴露和气道滴注均可对小鼠肝脏产生不利影响,且随着 PM2.5 浓度的增加损伤越严重,这可能与其诱导的氧化应激有关,且经气道滴注产生的损伤更严重.
语种：
中文
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Exposure to formaldehyde perturbs the mouse gut microbiome
作者：
Guo, Junhui;Zhao, Yun;Jiang, Xingpeng
（ ;Li, Rui;Xie, Hao;...
期刊：
Genes ,2018年9(4) ISSN：2073-4425
通讯作者：
Yang, Xu;Zhang, Luoping
作者机构：
[Xie, Bo; Ge, Leixin; Li, Rui; Yang, Xu; Zhao, Yun; Guo, Junhui] Cent China Normal Univ, Sch Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan 430079, Hubei, Peoples R China.;[Zhang, Luoping; Guo, Junhui] Univ Calif Berkeley, Sch Publ Hlth, Div Environm Hlth Sci, Berkeley, CA 94720 USA.;[Xie, Hao; Guo, Junhui] Wuhan Univ Technol, Sch Chem Chem Engn & Life Sci, Wuhan 430070, Hubei, Peoples R China.;[Jiang, Xingpeng] Cent China Normal Univ, Sch Comp, Wuhan 430079, Hubei, Peoples R China.
通讯机构：
[Yang, Xu] C;[Zhang, Luoping] U;Cent China Normal Univ, Sch Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan 430079, Hubei, Peoples R China.;Univ Calif Berkeley, Sch Publ Hlth, Div Environm Hlth Sci, Berkeley, CA 94720 USA.
关键词：
16s rRNA gene;Formaldehyde (FA);Gut microbiome;High-throughput;Murine model
摘要：
Exposure to Formaldehyde (FA) results in many pathophysiological symptoms, however the underlying mechanisms are not well understood. Given the complicated modulatory role of intestinal microbiota on human health, we hypothesized that interactions between FA and the gut microbiome may account for FA’s toxicity. Balb/c mice were allocated randomly to three groups: a control group, a methanol group (0.1 and 0.3 ng/mL MeOH subgroups), and an FA group (1 and 3 ng/mL FA subgroups). Groups of either three or six mice were used for the control or experiment. We applied high-throughput sequencing of 16S ribosomal RNA (rRNA) gene approaches and investigated possible alterations in the composition of mouse gut microbiota induced by FA. Changes in bacterial genera induced by FA exposure were identified. By analyzing KEGG metabolic pathways predicted by PICRUSt software, we also explored the potential metabolic changes, such as alpha-Linolenic acid metabolism and pathways in cancer, associated with FA exposure in mice. To the best of our knowledge, this preliminary study is the first to identify changes in the mouse gut microbiome after FA exposure, and to analyze the relevant potential metabolisms. The limitation of this study: this study is relatively small and needs to be further confirmed through a larger study. © 2018 by the authors.
语种：
英文
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Differential Health Effects of Constant versus Intermittent Exposure to Formaldehyde in Mice: Implications for Building Ventilation Strategies
作者：
Zhang, Xu;Zhao, Yun;Song, Jing;Yang, Xu;Zhang, Junfeng;...
期刊：
Environmental Science & Technology ,2018年52(3):1551-1560 ISSN：0013-936X
通讯作者：
Zhang, Yinping;Li, Rui
作者机构：
[Zhang, Xu; Zhang, Yinping] Tsinghua Univ, Dept Bldg Sci, Beijing 100084, Peoples R China.;[Zhang, Xu; Zhang, Yinping] Beijing Key Lab Indoor Air Qual Evaluat & Control, Beijing 100084, Peoples R China.;[Li, Rui; Yang, Xu; Zhao, Yun; Song, Jing] Cent China Normal Univ, Sch Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan 430079, Hubei, Peoples R China.;[Zhang, Junfeng] Duke Univ, Global Hlth Inst, Durham, NC USA.;[Zhang, Junfeng] Duke Univ, Nicholas Sch Environm, Durham, NC 27708 USA.
通讯机构：
[Zhang, Yinping] T;[Zhang, Yinping] B;[Li, Rui] C;Tsinghua Univ, Dept Bldg Sci, Beijing 100084, Peoples R China.;Beijing Key Lab Indoor Air Qual Evaluat & Control, Beijing 100084, Peoples R China.
摘要：
Formaldehyde, an air pollutant in the indoor environment, may have severe effects on human health. The aim of this study is to compare the health effects caused by intermittent exposure to formaldehyde (based on real monitoring) to those caused by exposures at constant concentration. Health effects explored in this study including the oxidative stress, histopathological changes, inflammatory responses, etc. Mice were divided into three groups and exposed to intermittent concentration formaldehyde (0.8 ppm for 12 h and 0 ppm for another 12 h), or constant concentration formaldehyde (0.4 ppm for 24 h) or zero concentration formaldehyde (reference) per day for 7, 14, and 28 days. Following these exposures, bronchoalveolar lavage fluid (BALF), lung tissue and lung tissue homogenate were prepared to measure biomarkers of oxidative stress (ROS, MDA, GSH), histopathological changes, inflammatory responses (EOS, NEU, LYM, IL-4, IL-5, IL-13, IL-6, IL-17A, NF-κB, IL-1β) and apoptosis (caspase-3). Compared to the constant exposure, intermittent exposure to fluctuating formaldehyde concentrations resulted in more profound increases in numbers of inflammatory cells in the BALF, greater biological alterations including apoptosis. The findings imply that with the same average indoor formaldehyde concentrations over the same time, a ventilation strategy to avoid higher peak concentrations would lead to lower health risks. © 2018 American Chemical Society.
语种：
英文
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邻苯二甲酸二异癸酯对小鼠学习记忆的影响
作者：
路雨;李瑶;胡赢丹;李秋林;赵云;...
期刊：
中国环境科学 ,2018年38(1):361-368 ISSN：1000-6923
通讯作者：
Li, Rui(ruli@mail.ccnu.edu.cn)
作者机构：
[路雨; 李瑶; 胡赢丹; 李秋林; 赵云; 邹鉴; 刘潇童; 杨旭; 李睿] 华中师范大学生命科学学院, 遗传调控与整合生物学湖北省重点实验室, 湖北, 武汉, 430079
通讯机构：
Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, Wuhan, China
关键词：
邻苯二甲酸二异癸酯;学习记忆;氧化损伤;白藜芦醇;Morris水迷宫
摘要：
为研究增塑剂邻苯二甲酸二异癸酯(DIDP)对小鼠学习和记忆能力的影响,以白藜芦醇(Res)作为保护剂,将42只雄性昆明小鼠随机分为6组,每组7只,分别为:生理盐水组、1.5,15,150 mg/(kg·d) DIDP组、20 mg/(kg·d) Res组、150 mg/(kg·d) DIDP+20 mg/(kg·d) Res组.连续灌胃染毒9d,期间同时进行Morris水迷宫实验.第10 d将小鼠处死,取出脑组织,检测活性氧簇(ROS)、谷胱甘肽(GSH)、丙二醛(MDA)、8-羟基脱氧鸟苷(8-OHdG)、肿瘤坏死因子(TNF-α)、白细胞介素1β(IL-1β)的含量.并对小鼠海马体切片进行H&E染色,观察病理变化.结果显示,15,150 mg/(kg·d) DIDP染毒可导致小鼠的学习和记忆能力显著低于对照组,同时可诱发脑组织产生氧化应激,并促进炎症因子释放,而Res能有效减弱脑组织氧化应激水平.由上可得,DIDP致小鼠学习和记忆能力下降可能与其引起的脑组织中海马体的氧化损伤有关,同时Res可能通过降低DIDP引起的氧化应激进而减轻其对小鼠造成的学习记忆损伤.
语种：
中文
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DIDP通过线粒体- Caspase途径诱导昆明小鼠肝脏损伤的研究
作者：
李瑶;路雨;胡赢丹;李秋林;赵云;...
期刊：
环境科学研究 ,2018年31(11):1957-1964 ISSN：1001-6929
通讯作者：
Li, R.
作者机构：
[李瑶; 路雨; 胡赢丹; 李秋林; 赵云; 李睿] 华中师范大学, 遗传调控与整合生物学湖北省重点实验室, 湖北, 武汉, 430079
通讯机构：
Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, Wuhan, China
关键词：
邻苯二甲酸二异癸酯;氧化应激;线粒体损伤;细胞凋亡;肝脏
摘要：
为探究DIDP（Di-iso-decyl phthalate,邻苯二甲酸二异癸酯）对肝脏的影响及其可能的分子机制,以昆明小鼠为研究对象,选用Res（resveratrol,白藜芦醇）为抗氧化剂,分别设置对照组,0. 15、1. 5、15、150 mg/（kg·d）DIDP组,Res组,150 mg/（kg·d）DIDP+Res组,灌胃染毒9 d后,对小鼠肝脏切片进行HE染色观察,并检测ROS（reactive oxygen,活性氧）、GSH（glutathione,谷胱甘肽）、MDA（malondialdehyde,丙二醛）、Cyt-C（cytochromec,细胞色素C）、Caspase-3和血清中的ALT（alanine aminotransferase,丙氨酸氨基转移酶）含量.结果表明:与对照组相比,15、150 mg/（kg·d）DIDP组小鼠血清中ALT含量极显著上升（P<0. 01）;HE染色结果显示,15、150 mg/（kg·d）DIDP组小鼠出现肝细胞水肿、肝索紊乱、肝窦以及肝中央静脉扩张等现象;15、150 mg/（kg·d）DIDP组小鼠肝脏ROS含量显著上升（P<0. 05）,GSH含量显著下降（P<0. 05）,150 mg/（kg·d）DIDP组小鼠肝脏MDA含量极显著上升（P<0. 01）;1. 5、15、150 mg/（kg·d） DIDP组小鼠肝脏中c （Cyt-C）极显著上升（P <0. 01）;15、150 mg/（kg·d） DIDP组小鼠肝脏中Caspase-3表达量极显著上升（P<0. 01）. DIDP染毒剂量的增加对肝脏的各种损伤程度呈上升趋势,Res可减轻上述DIDP对肝脏造成的各种损伤.研究显示,15、150 mg/（kg·d）DIDP可诱导肝脏组织氧化应激水平上升,进而造成线粒体损伤,导致细胞凋亡,造成肝功能受损,因此,线粒体-Caspase途径可能是DIDP诱导肝脏损伤的潜在机制之一.
语种：
中文
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PM_(2.5)和甲醛联合暴露致小鼠肺损伤及其分子机制的研究
作者：
閤静;赵云;黄佳伟;张萍;潘雯;...
期刊：
生态毒理学报 ,2018年13(3):87-93 ISSN：1673-5897
作者机构：
[閤静; 赵云; 黄佳伟; 张萍; 潘雯; 尤安琪; 黄希; 杨旭; 李睿] 华中师范大学生命科学学院, 武汉, 430079
关键词：
甲醛;复合暴露;肺组织损伤;分子机制
摘要：
我国城市当前普遍存在室外大气PM_(2.5)与室内甲醛(FA)联合污染状况,二者均被报道在单独暴露下可以导致肺损伤并诱导和诱发哮喘的急性发作,但其联合污染的具体效应,以及分子机制目前尚不清楚。为探究PM_(2.5)和/或甲醛暴露对小鼠的肺损伤及其可能的机制,分别将雄性Balb/c小鼠分为以下6组:对照组,AZD8055组,PM_(2.5)组,FA组,PM_(2.5) +FA组,PM_(2.5) +FA+ AZD8055组。染毒结束后,观察肺组织病理学变化;检测肺组织氧化损伤,活性氧(reactive oxygen species, ROS),还原型谷胱甘肽(glutathione, GSH)和丙二醛(malondialdehyde, MDA)的含量,DNA损伤,DNA-蛋白质交联( DNA-protein crosslink,DPC)系数和8羟基脱氧鸟苷(8-OH-dG)的含量,以及细胞凋亡、半胱氨酸天冬氨酸蛋白酶-3(Caspase-3)的含量。结果表明,当吸入气态甲醛浓度为3 mg·m~(-3),气道滴注PM_(2.5)浓度为2.5 mg·mL~(-1)时,肺组织出现不同程度的支气管重塑和炎症细胞浸润。ROS显著上升,GSH显著下降,DPC、8-OH-dG以及Caspase-3都显著上升。添加AZD8055后,肺组织损伤效应更加显著。PM_(2.5)复合甲醛的暴露导致小鼠肺损伤具有协同作用,氧化应激及其下游的DNA损伤可能是甲醛联合PM_(2.5)致小鼠肺损伤的一种重要机制。
语种：
中文
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Oral exposure to diisodecyl phthalate aggravates allergic dermatitis by oxidative stress and enhancement of thymic stromal lymphopoietin
作者：
Shen, Shiping;Li, Jinquan;You, Huihui;Wu, Zhuo;Wu, Yang;...
期刊：
Food and Chemical Toxicology ,2017年99:60-69 ISSN：0278-6915
通讯作者：
Yang, Xu;Chen, Mingqing
作者机构：
[Guo, Qing; Shen, Shiping; Li, Jinquan; Chen, Mingqing; Li, Rui; You, Huihui; Li, Xiaoxiao; Yang, Xu; Zhao, Yun; Wu, Zhuo; Zhu, Yuqing; Yang, X; Chen, MQ] Cent China Normal Univ, Sch Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan 430079, Hubei, Peoples R China.;[Zhao, Yun] Hubei Univ Sci & Technol, Coll Basic Med Sci, Xianning 437100, Peoples R China.
通讯机构：
[Yang, X; Chen, MQ] C;Cent China Normal Univ, Sch Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan 430079, Hubei, Peoples R China.
关键词：
Allergic contact dermatitis;Diisodecyl phthalate (DIDP);NF-kappa B;Oxidative stress;Thymic stromal lymphopoietin (TSLP)
摘要：
Diisodecyl phthalate (DIDP) is extensively used as an environmentally friendly plasticizer. However, little is known about the adverse effects and the underlying mechanisms of DIDP exposure on immunological diseases. We aimed to determine the role and mechanisms of DIDP exposure in allergic contact dermatitis-like skin lesions. We show that oral DIDP exposure can aggravate allergic dermatitis in mice. Moreover, an increase of ROS, total serum IgE and IL-4 levels were concomitant with this deterioration. We detected the expression of Thymic stromal lymphopoietin (TSLP) and the activation of STATs and NF-kappa B signal pathways. The data indicated that DIDP in combination with FITC triggers TSLP production. Our results also suggested that DIDP exacerbated the activation of NF-kappa B signal pathways, with an enhancement in TSLP expression, which potentiated the activation of STATs and the degranulation of mast cells in the skin, and finally exacerbated allergic dermatitis. The study also suggested that melatonin enhanced the expression of Nrf2, up-regulated the antioxidant genes HO-1 and NQO1, reduced the levels of oxidative stress and TSLP, and alleviated allergic dermatitis. The results demonstrated that DIDP exacerbated allergic dermatitis through oxidative stress and enhanced TSLP production. (C) 2016 Elsevier Ltd. All rights reserved.
语种：
英文
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PM2.5和甲醛复合暴露致小鼠造血毒性及其分子机制的研究
作者：
閤静;杨旭;李睿
作者机构：
[閤静; 杨旭; 李睿] 华中师范大学生命科学学院
会议名称：
2017环境与公共健康学术会议暨中国环境科学学会环境医学与健康分会、中国毒理学会生化与分子毒理专业委员会2017年年会
会议时间：
2017-11-10
会议地点：
中国广东广州
关键词：
甲醛;复合暴露;造血毒性;分子机制
摘要：
我国城市当前普遍存在大气PM2.5与室内甲醛复合污染状况,二者均被报道在单独暴露可引起造血毒性[1,2],但分子机制尚不清楚。为探究FA复合PM2.5对小鼠造血毒性的影响及其可能机制,分别从血液,造血器官（骨髓,脾脏）,髓系祖细胞三个层面进行系统研究。将雄性Balb/c小鼠分别暴露于PM2.5和/或甲醛中。结果表明,小鼠骨髓、脾脏出现不同程度病理学变化,减少了外周血血细胞的数量和
语种：
中文
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