Rosiglitazone inhibits PM2.5-induced cytotoxicity in human lung epithelial A549 cells

Peansukwech

2020

Heliyon

Background: This model demonstrated the correlation between lung cancer incidences and the parts of ambient air pollution according to the National Aeronautics and Space Administration (NASA)'s high resolution technology satellites. Methods: Chemical type of aerosols was investigated by the Aerosol Diagnostics Model such as black carbon, mineral dust, organic carbon, sea-salt and SO4. The model investigated associations between the six year accumulation of each aerosol and lung cancer incidence by Bayesian hierarchical spatio-temporal model. Which also represented integrated geophysical parameters. Results: In analyses of accumulated chemical aerosol component from 2010 -2016, the incidence rate ratio (IRR) of patients in 2017 were estimated. We observed a significant increasing risk for organic carbon exposure (IRR 1.021, 95%CI 1.020-1.022), SO 4 , (IRR 1.026, 95% CI 1.025-1.028) and dust, (IRR 1.061, 95% CI 1.058-1.064). There was also suggestion of an increased risk with, every 1 ug/m 3 increase in organic carbon compound is associated with 21% increased risk of lung cancer, whereas a 26% excess risk of cancer per 1 ug/m 3 increase in mean SO 4 and 61% increased risk of lung cancer for dust levels. The other variables were the negative IRR which did not increase the risk of the exposed group. Conclusion: With our results, this process can determine that organic carbon, SO 4 and dust was significantly associated with the elevated risk of lung cancer.

Section: Discussionmentioning

confidence: 99%

Construction of polluted aerosol in accumulation that affects the incidence of lung cancer

Peansukwech

2020

Heliyon

“…It has been demonstrated that PM, especially PM2.5, have the capacity to reduce cell proliferation , through cell cycle arrest in different types of cells. ,,,− PM are also known to induce apoptosis and autophagy. ,− Interestingly, a crosstalk between the latter has been documented, , and both can be explained by PM2.5 implication concerning a decrease of mRNA and protein level of mammalian target of rapamycin (mTOR). − Quite relevant, PM2.5-induced apoptosis was found to be mediated by an increase of known apoptotic factors like p53 and a decrease of its inhibitor, SGK1 usually activated by mTOR, resulting in a cascade of different steps and involving a series of molecules such as Bax, cytochrome c , APAF-1, and caspases (Figure ). − Of course, additional studies are required in order to determine the relevance of these speculations.…”

Section: Pathogenic Impact Of Soamentioning

confidence: 99%

Pathogenic Mechanisms of Secondary Organic Aerosols

Déméautis

Delles

Tomaz

et al. 2022

Chem. Res. Toxicol.

Air pollution represents a major health problem and an economic burden. In recent years, advances in air pollution research has allowed particle fractionation and identification of secondary organic aerosol (SOA). SOA is formed from either biogenic or anthropogenic emissions, through a mass transfer from the gaseous mass to the particulate phase in the atmosphere. They can have deleterious impact on health and the mortality of individuals with chronic inflammatory diseases. The pleiotropic effects of SOA could involve different and interconnected pathogenic mechanisms ranging from oxidative stress, inflammation, and immune system dysfunction. The purpose of this review is to present recent findings about SOA pathogenic roles and potential underlying mechanisms focusing on the lungs; the latter being the primary exposed organ to atmospheric pollutants.

“…Medium without FC was used as a control. The PM2.5 doses were determined based on previous studies [ 43 , 44 ]. Cells were collected after stimulation for 0.5 h, 1 h, 2 h, and 6 h. All the experiments were repeated in triplicate.…”

Section: Methodsmentioning

confidence: 99%

A Novel Herbal Extract Blend Product Prevents Particulate Matters-Induced Inflammation by Improving Gut Microbiota and Maintaining the Integrity of the Intestinal Barrier

et al. 2022

Air pollutants of PM2.5 can alter the composition of gut microbiota and lead to inflammation in the lung and gastrointestinal tract. The aim of this study was to evaluate the protective effect of a novel herbal extract blend, FC, composed of Lonicera japonica extract, Momordica grosvenori extract, and broccoli seed extract, on PM2.5-induced inflammation in the respiratory and intestinal tract. A549 cells and THP-1 cells, as well as C57BL/6 mice, were stimulated with PM2.5 to establish in vitro and in vivo exposure models. The models were treated with or without FC. The expression of inflammatory cytokines and tight junction proteins were studied. Proteomic analysis was performed to elucidate mechanisms. Mouse feces were collected for gut microbiota analysis. FC was shown to modulate the upregulation of pro-inflammatory cytokines mRNA expression in A549 and THP-1 cells and downregulated tight junction proteins mRNA expression in A549 cells due to PM2.5 stimulation. In animal models, the decreased expression of the anti-inflammatory factor il-10, tight junction protein ZO-1, and the elevated expression of COX-2 induced by PM2.5 were improved by FC intervention, which may be associated with zo-1 and cox-2 signaling pathways. In addition, FC was shown to improve the gut microbiota by increasing the abundance of beneficial bacteria.