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Effects of Combined Exposure to Formaldehyde and PM2.5 on the Brain of Balb/c Mice Asthma Model

生态毒理学报 2018年第6期13卷 124-135页

作者： andrea stojkoska Song Jing Kang Jun Liu Xudong Shuai Menglei Li Yong Zhao Liang Yang Xu Hubei Key Laboratory of Genetic Regulation and Integrative Biology School of Life SciencesCentral China Normal UniversityWuhan 430079China

Epidemiological studies have shown that there is a link between asthma and brain damage,but toxicological studies have not fully confirmed yet,especially the effects of asthma on the brain. In this study,at first,we explore the effects of asthma on the brain through the establishment of an allergic asthma model. Then PM_(2.5),a typical outdoor air pollutant and formaldehyde,a typical indoor air pollutant were selected to be closer to the true environment and find whether there is any synergism between them. In this study,an ovalbumin( OVA)-sensitized mice asthma model was established. 30 male Balb/c mice were randomly divided into 5 groups:( 1) saline control group,( 2) OVA-sensitized group,( 3) OVA-combined with formaldehyde exposure group,( 4) OVA-combined with PM_(2.5) exposure group,( 5) Combination of OVA,formaldehyde and PM_(2.5) exposure group. The mice were inhaled with formaldehyde or/and instilled with PM_(2.5) from day 1 to 18. The mice asthma model was developed by OVA sensitization and challenge. The mice were sensitized with OVA+Al( OH)3( 5 mg OVA and 175 mg Al( OH)3 in 30 m L saline each time) or saline( 30 m L saline each time) by intraperitoneal injection on day 1,7 and *** was then followed by an aerosol challenge in 1% OVA( 30 min·d^(-1)) from day 19 to 25( 7 times) using an ultrasonic nebulizer. On the 26 th day,the organ coefficient of mice brain was counted,then the contents of oxidative stress of mice brain were measured,including reactive oxygen species( ROS),glutathione( GSH) and malondialdehyde( MDA),and the concentrations of NF-κB and interleukin-1β( IL-1β) were detected by using ELISA *** of interleukin-6( IL-6) was made with immunohistochemical method. Histological assay for brain was also conducted. In our results,all the OVA treated groups showed a significant increase of ROS and a significant decrease of GSH contents when compared with the control group. Except OVA-sensitized group,other OVA treated groups also showed a

关键词： formaldehyde PM2.5 brain allergic asthma oxidative stress

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Mycobacterium Lrp/AsnC family transcriptional factor modulates the arginase pathway as both a sensor and a transcriptional repressor

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Journal of Genetics and Genomics 2021年第11期48卷 1020-1031页

作者： Shuangquan Yan Junfeng Zhen Yuzhu Li Yu Huang Xuefeng Ai Yue Li andrea stojkoska Xue Huang Cao Ruan Jiang Li Lin Fan Jianping Xie Institute of Modern Biopharmaceuticals State Key Laboratory Breeding Base of Eco-Environment and Bio-Resource of the Three Gorges AreaKey Laboratory of Ministry of Education Eco-Environment of the Three Gorges Reservoir RegionSchool of Life SciencesSouthwest UniversityChongqing 400715China Shanghai Clinic and Research Center of Tuberculosis Shanghai Pulmonary HospitalTongji University School of MedicineShanghai Key Laboratory of TuberculosisShanghai 200433China

L-Arginine is the precursor of nitric oxide(NO),a host immune effector against intracellular pathogens including Mycobacterium tuberculosis(***).Pathogens including *** have evolved various strategies targeting arginine to block the production of NO for better survival and ***,L-arginine metabolism and regulation in Mycobacterium are poorly ***,we report the identification of *** MSMEG_1415(homolog of *** Rv2324)as an arginine-responsive transcriptional factor regulating the arginase *** the absence of L-arginine,MSMEG_1415 acts as a repressor to inhibit the transcription of the roc(for arginine,ornithine catabolism)gene cluster,thereby switching off the arginase *** with L-arginine relieves the transcriptional inhibition of MSMEG_1415 on the roc gene cluster to activate the arginase ***,the L-arginine-MSMEG_1415 complex activates the transcription of the roc gene cluster by recognizing and binding a 15-bp palindrome motif,thereby preventing the excess accumulation of L-arginine in ***,MSMEG_1415 confers mycobacteria resistance to starvation and fluoroquinolones exposure,suggestive of its important role in *** *** results uncover a unique regulatory mechanism of arginine metabolism in mycobacteria and identify *** Rv2324 as an attractive candidate target for the design of drugs against tuberculosis.

关键词： Mycobacterium tuberculosis Lrp/AsnC family transcriptional regulator Repressor Arginine Arginase pathway Persistence

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甲醛和PM2.5联合暴露对Balb/c小鼠过敏性哮喘模型脑组织的影响

甲醛和PM2.5联合暴露对Balb/c小鼠过敏性哮喘模型脑组织的影响

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作者： andrea stojkoska 华中师范大学

学位级别：硕士

流行病学研究表明哮喘与脑损伤之间存在联系,但毒理学研究尚未完全证实,特别是哮喘对脑组织是否存在影响。本研究首先建立Balb/c过敏性哮喘小鼠模型,通过测定小鼠脑组织氧化应激的水平,包括活性氧(ROS)、谷胱甘肽(GSH)和丙二醛(MDA),同... 详细信息

流行病学研究表明哮喘与脑损伤之间存在联系,但毒理学研究尚未完全证实,特别是哮喘对脑组织是否存在影响。本研究首先建立Balb/c过敏性哮喘小鼠模型,通过测定小鼠脑组织氧化应激的水平,包括活性氧(ROS)、谷胱甘肽(GSH)和丙二醛(MDA),同时观察小鼠脑组织病理学变化和炎症反应相关指标的含量变化,包括核因子κB(NF-κB)、白介素-1β和白细胞介素-6,以此探讨过敏性哮喘对小鼠脑组织的影响。结果显示过敏性哮喘可以通过氧化应激反应对小鼠脑组织造成损伤。众所周知,环境污染物对疾病的影响不容忽视,但以往的研究大多集中在单一污染物上,忽略了混合污染物的影响。同时,在这项研究中,选择典型的室外空气污染物——PM2.5和典型的室内空气污染物——甲醛进行联合暴露,以此更接近真实的环境,并观察这两种典型污染物之间是否具有一定的协同作用。结果表明,暴露于甲醛和PM2.5会增加过敏性哮喘对小鼠脑组织造成的损伤,这可能是由氧化应激和活化的NF-κB介导,从而促进炎性因子的释放导致炎症增强。

关键词：甲醛 PM2.5 脑

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