Toxicology Letters, Journal Year: 2020, Volume and Issue: 331, P. 208 - 217
Published: June 20, 2020
Language: Английский
Toxicology Letters, Journal Year: 2020, Volume and Issue: 331, P. 208 - 217
Published: June 20, 2020
Language: Английский
Ecotoxicology and Environmental Safety, Journal Year: 2019, Volume and Issue: 174, P. 344 - 352
Published: March 5, 2019
Language: Английский
Citations
249International 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
176Journal of Hazardous Materials, Journal Year: 2021, Volume and Issue: 421, P. 126760 - 126760
Published: July 27, 2021
Language: Английский
Citations
105International Immunopharmacology, Journal Year: 2022, Volume and Issue: 112, P. 109186 - 109186
Published: Sept. 15, 2022
Language: Английский
Citations
87Chronic 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
146Chemosphere, Journal Year: 2020, Volume and Issue: 264, P. 128436 - 128436
Published: Sept. 29, 2020
Language: Английский
Citations
117Scientific 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
113Environmental 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
95Toxicology Letters, Journal Year: 2018, Volume and Issue: 290, P. 123 - 132
Published: March 20, 2018
Language: Английский
Citations
90Ecotoxicology and Environmental Safety, Journal Year: 2019, Volume and Issue: 182, P. 109425 - 109425
Published: July 8, 2019
Language: Английский
Citations
78