Ambient PM2.5 chronic exposure leads to cognitive decline in mice: From pulmonary to neuronal inflammation DOI

Yikai Shou,

Xiaozheng Zhu,

Danna Zhu

et al.

Toxicology Letters, Journal Year: 2020, Volume and Issue: 331, P. 208 - 217

Published: June 20, 2020

Language: Английский

A review of the possible associations between ambient PM2.5 exposures and the development of Alzheimer's disease DOI

Yikai Shou,

Yilu Huang,

Xiaozheng Zhu

et al.

Ecotoxicology and Environmental Safety, Journal Year: 2019, Volume and Issue: 174, P. 344 - 352

Published: March 5, 2019

Language: Английский

Citations

249

In Vitro and In Vivo Experimental Studies of PM2.5 on Disease Progression DOI Open Access
Ching-Chang Cho,

Wen-Yeh Hsieh,

Chin-Hung Tsai

et al.

International Journal of Environmental Research and Public Health, Journal Year: 2018, Volume and Issue: 15(7), P. 1380 - 1380

Published: July 1, 2018

Air pollution is a very critical issue worldwide, particularly in developing countries. Particulate matter (PM) type of air that comprises heterogeneous mixture different particle sizes and chemical compositions. There are various sources fine PM (PM2.5), the components may also have effects on people. The pathogenesis PM2.5 several diseases remains to be clarified. long history epidemiological research diseases. Numerous studies show can induce variety chronic diseases, such as respiratory system damage, cardiovascular dysfunction, diabetes mellitus. However, evidence associated with potential mechanisms progression need proved precisely through vitro vivo investigations. Suggested lead adverse include increasing oxidative stress, inflammatory responses, genotoxicity. aim this review provide brief overview experimental from last decade. summarized results could clear information about PM2.5-induced disease.

Language: Английский

Citations

176

Biomarkers for the adverse effects on respiratory system health associated with atmospheric particulate matter exposure DOI
Caixia Guo,

Songqing Lv,

Yufan Liu

et al.

Journal of Hazardous Materials, Journal Year: 2021, Volume and Issue: 421, P. 126760 - 126760

Published: July 27, 2021

Language: Английский

Citations

105

Astragaloside IV regulates the ferroptosis signaling pathway via the Nrf2/SLC7A11/GPX4 axis to inhibit PM2.5-mediated lung injury in mice DOI
Xiaoming Wang, Yilan Wang, Demei Huang

et al.

International Immunopharmacology, Journal Year: 2022, Volume and Issue: 112, P. 109186 - 109186

Published: Sept. 15, 2022

Language: Английский

Citations

87

Fine particulate matter (PM2.5): The culprit for chronic lung diseases in China DOI Creative Commons
Tao Li, Rong Hu, Zi Chen

et al.

Chronic Diseases and Translational Medicine, Journal Year: 2018, Volume and Issue: 4(3), P. 176 - 186

Published: Aug. 29, 2018

Air pollution is a world public health problem. Particulate matter (PM), mix of solid and liquid particles in the air, becomes an increasing concern social economic development China. For decades, epidemiological studies have confirmed association between fine particle pollutants respiratory diseases. It has been reported different populations that increased Fine particulate (PM2.5) concentrations cause elevated susceptibility to diseases, including acute distress, asthma, chronic obstructive pulmonary disease, lung cancer. This review will discuss pathophysiology PM2.5 which are helpful for prevention air treatment tract inflammatory

Language: Английский

Citations

146

Effects of PM2.5 exposure on reproductive system and its mechanisms DOI
Lingjuan Wang, Dan Luo, Xiaolong Liu

et al.

Chemosphere, Journal Year: 2020, Volume and Issue: 264, P. 128436 - 128436

Published: Sept. 29, 2020

Language: Английский

Citations

117

Urban PM2.5 exacerbates allergic inflammation in the murine lung via a TLR2/TLR4/MyD88-signaling pathway DOI Creative Commons

Miao He,

Takamichi Ichinose,

Yasuhiro Yoshida

et al.

Scientific Reports, Journal Year: 2017, Volume and Issue: 7(1)

Published: Sept. 4, 2017

Nevertheless its mechanism has not been well explained yet, PM2.5 is recognized to exacerbate asthma. In the present study, roles of toll-like receptor (TLR) 2, TLR4 and MyD88, in exacerbation allergen-induced lung eosinophilia caused by urban was investigated. TLR2-, TLR4-, MyD88-deficient WT BALB/c mice were intratracheally challenged with +/- ovalbumin (OVA) four times at 2-week intervals. increased neutrophil numbers KC bronchoalveolar lavage fluid slight peribronchiolar inflammation mice. However, these changes attenuated, but completely suppressed gene-deficient mice, especially MyD88-/- + OVA exacerbated OVA-related eosinophilia. This includes increase IL-5, IL-13, eotaxin MCP-3; infiltration eosinophils into airway submucosa; proliferation goblet cells epithelium; production antigen-specific IgE IgG1 serum. All effects stronger TLR2-/- than TLR4-/- this pro-inflammatory mediator-inducing ability considerably weak pathology negligible. These results suggest that may allergic murine via a TLR2/TLR4/MyD88-signaling pathway. PM2.5-bound trace microbial elements, such as lipopolysaccharide be strong candidate for

Language: Английский

Citations

113

PM2.5 exposure induces systemic inflammation and oxidative stress in an intracranial atherosclerosis rat model DOI
Longfei Guan, Xiaokun Geng, Christopher Stone

et al.

Environmental Toxicology, Journal Year: 2019, Volume and Issue: 34(4), P. 530 - 538

Published: Jan. 23, 2019

Abstract Objectives Exposure to airborne particle (PM 2.5 ) is a risk factor for intracranial atherosclerosis (ICA). Because of the established role systemic inflammation and oxidative stress by PM , we determined whether these processes account ‐mediated ICA, also omega‐3 fatty acid (O3FA) dietary supplementation could attenuate them. Methods Adult Sprague‐Dawley rats were exposed filtered air (FA) or fed either normal chow diet (NCD) high‐cholesterol (HCD), administered with without O3FA (5 mg/kg/day gavage) 12 weeks. The lumen thickness middle cerebral artery (MCA) assessed. Serum tumor necrosis alpha (TNF‐α), interleukin 6 (IL‐6), interleukin‐1β (IL‐1β), interferon gamma (IFN‐γ) detected ELISA. Reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) activity, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) mRNA levels Nrf2, HO‐1, NQO‐1, protein level NOX subunit gp91 quantified determine profile brain vessels. Results increased ( P < .05) especially in HCD group; elevated serum TNF‐α, IL‐6, IL‐1β, IFN‐γ; cerebrovascular ROS, MDA, levels; decreased SOD activity. Nrf2 HO‐1 NQO‐1 upregulated exposure, group. attenuated ‐induced inflammation, vascular injury, ICA. Conclusions exposure induced ICA HCD. prevented development, may therefore exert protective effect against atherogenic potential .

Language: Английский

Citations

95

Air pollution is associated with the development of atherosclerosis via the cooperation of CD36 and NLRP3 inflammasome in ApoE -/- mice DOI
Xihao Du, Shuo Jiang,

Xuejiao Zeng

et al.

Toxicology Letters, Journal Year: 2018, Volume and Issue: 290, P. 123 - 132

Published: March 20, 2018

Language: Английский

Citations

90

Resveratrol alleviates chronic “real-world” ambient particulate matter-induced lung inflammation and fibrosis by inhibiting NLRP3 inflammasome activation in mice DOI
Shibin Ding,

Huifeng Wang,

Mengruo Wang

et al.

Ecotoxicology and Environmental Safety, Journal Year: 2019, Volume and Issue: 182, P. 109425 - 109425

Published: July 8, 2019

Language: Английский

Citations

78