Air-pollutant particulate matter 2.5 (PM2.5)-induced inflammation and oxidative stress in diseases: Possible therapeutic approaches DOI Creative Commons
Asish K. Ghosh

International Journal of Science and Research Archive, Год журнала: 2024, Номер 11(1), С. 2148 - 2162

Опубликована: Фев. 18, 2024

Today, air pollution is one of the greatest threats to organismal healthspan. The environmental earth contaminated with a wide variety artificially generated pollutants like fine particulate matter (PM2.5) emitting from industry, fuel engine vehicles, biomass combustion, fumes blasting, crop residue burning, and wildfire. pollutant PM2.5 induces massive oxidative stress inflammation, major contributors in initiation progression numerous diseases including pulmonary, cardiovascular, renal, hepatic, reproductive, neurological, mental, accelerated biological aging. provocative question following: how can we solve this associated problem? As it not realistic clean environment at once toxic pollution, initiatives have been undertaken develop novel therapeutic approaches control air-pollutant-induced inflammation devastating diseases. primary goal review article discuss systematically key findings recent preclinical studies documenting first, role augmentation stress, diseases; second, efficacies different natural synthetic compounds amelioration PM2.5-induced pyroptosis, pathologies. Further investigation on safety these will be helpful select effective non-toxic compound(s) for clinical trial drug development.

Язык: Английский

Air pollution and skin diseases: A comprehensive evaluation of the associated mechanism DOI Creative Commons
Xiaoyu Gu, Zhengrui Li, Juan Su

и другие.

Ecotoxicology and Environmental Safety, Год журнала: 2024, Номер 278, С. 116429 - 116429

Опубликована: Май 7, 2024

Air pollutants deteriorate the survival environment and endanger human health around world. A large number of studies have confirmed that air pollution jeopardizes multiple organs, such as cardiovascular, respiratory, central nervous systems. Skin is largest organ first barrier protects us from outside particulate matter (PM), polycyclic aromatic hydrocarbons (PAHs), volatile organic compounds (VOCs) will affect structure function skin bring about development inflammatory diseases (atopic dermatitis (AD), psoriasis), accessory (acne, alopecia), auto-immune (cutaneous lupus erythematosus(CLE) scleroderma), even tumors (melanoma, basal cell carcinoma (BCC), squamous-cell (SCC)). Oxidative stress, damage, microbiome dysbiosis, inflammation are pathogenesis stimulation. In this review, we summarize current evidence on effects possible mechanisms to provide strategies for future research.

Язык: Английский

Процитировано

19
Network pharmacology and phytochemical composition combined with validation in vivo and in vitro reveal the mechanism of platycodonis radix ameliorating PM2.5-induced acute lung injury DOI

Xianlei Han,

Yue Zhang, Fan Zhang

и другие.

Journal of Ethnopharmacology, Год журнала: 2024, Номер 337, С. 118829 - 118829

Опубликована: Сен. 13, 2024

Язык: Английский

Процитировано

6
PM2.5 induces renal tubular injury by activating NLRP3-mediated pyroptosis DOI Creative Commons
Weilin Chen,

Yanfang Luo,

Jingjing Quan

и другие.

Ecotoxicology and Environmental Safety, Год журнала: 2023, Номер 265, С. 115490 - 115490

Опубликована: Сен. 23, 2023

Fine particulate matter (PM2.5)-related health issues have received increasing attention as a worldwide public problem, and PM2.5-related chronic kidney disease (CKD) has been emerging over the years. Limited research focused on mechanism of PM2.5-induced disease. To investigate impact PM2.5 its potential mechanism, we generated PM2.5-exposed C57BL/6 mouse model by using Shanghai Meteorological Environment Animal Exposure System (Shanghai-METAS) for 12 weeks, urine, blood tissues were collected. The pathological changes function measured after exposure weeks. Along with glomerular damage, tubular damage was also severe in mice. results mRNA-seq indicate that pyroptosis is involved. Pyroptosis defined caspase-1-dependent programmed cell death response to insults. expression nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3), Caspase-1, gasdermin D (GSDMD) IL-1β detected. NLRP3 inflammasome activation subsequent observed Bumpt cells too. At meantime, inhibitors caspase-1 applied exposed cells. It turned out significant rescue effect inhibitors. This study revealed new insights into injury specific well morphological changes, important role dysfunction.

Язык: Английский

Процитировано

10
The role of pyroptosis in environmental pollutants-induced multisystem toxicities DOI
Rui Xu, Longfei Li,

Yijia Ke

и другие.

Life Sciences, Год журнала: 2025, Номер 372, С. 123632 - 123632

Опубликована: Апрель 10, 2025

Язык: Английский

Процитировано

0
Fudosteine attenuates lung inflammation in mice with PM2.5-induced asthma exacerbation by inhibiting pyroptosis via the NLRP3/caspase-1/GSDMD pathway DOI
Jianling Liu, Zhongpeng Li, Zhongyi Li

и другие.

Toxicology and Applied Pharmacology, Год журнала: 2025, Номер unknown, С. 117346 - 117346

Опубликована: Апрель 1, 2025

Язык: Английский

Процитировано

0
Human dental pulp stem cells attenuate airway inflammation in mice with PM2.5-induced asthma exacerbation by inhibiting the pyroptosis pathway DOI Creative Commons
Jianling Liu, Yuehua Chen,

Zhongpeng Li

и другие.

Stem Cell Research & Therapy, Год журнала: 2025, Номер 16(1)

Опубликована: Май 13, 2025

Fine particulate matter (PM2.5) exposure significantly exacerbates respiratory morbidity, particularly in asthmatic individuals, highlighting an urgent need for effective therapeutic interventions. In this study, we evaluated the potential and underlying mechanisms of human dental pulp stem cells (hDPSCs), a promising mesenchymal cell population, mitigating airway inflammation mice with PM2.5-induced asthma exacerbation. PM2.5-exacerbated ovalbumin (OVA)-asthma murine model, hDPSCs were intravenously administered MCC950 (NLRP3 inhibitor) as positive control, systematically evaluating their effects on pyroptosis through pulmonary function tests, histopathological examination, cytological molecular analyses. The administration ameliorated inflammation. Moreover, further alleviated Th2 decreased serum IgE concentrations, along decrease eosinophils BALF. At same time, interleukin-1β (IL-1β) IL-18 levels BALF caspase-1 activity lung tissues reduced. addition, immunohistochemistry showed that expression NLRP3, caspase-1, GSDMD, cleaved capsase-1 IL-1β western blot results also level NLRP3/caspase-1/GSDMD/cleaved classical pathway after intervention. These findings provided first evidence transplantation attenuated allergic mucus secretion Thus, exert these protective suppression NLRP3/caspase-1/GSDMD-mediated pathway, suggesting novel cell-based therapy PM2.5 inhalation-mediated asthma.

Язык: Английский

Процитировано

0
Air-pollutant Particulate Matter 2.5 (PM2.5)-induced Inflammation and Oxidative Stress in Diseases: Possible Therapeutic Approaches DOI Open Access
Asish K. Ghosh

Опубликована: Дек. 20, 2023

Today, air pollution is the greatest threat to organismal healthspan. The environment of our planet earth, habitat over eight billion humans and estimated twenty billions other animals, contaminated with a wide variety pollutants. Unfortunately, humans, out living organisms on are solely responsible for polluting through emitting pollutants like particulate matter from industry, fuel engine vehicles, biomass combustion, toxic fumes blasting, wildfire. In modern world, human-caused induce massive oxidative stress inflammation, major contributors in initiation progression many diseases including pulmonary, cardiovascular, renal, hepatic, reproductive, neurological, mental, accelerated biological aging. provocative question following: how can we solve this human-created problem? As it not realistic clean at once pollution, initiatives have been undertaken develop novel therapeutic approaches control air-pollutant-induced inflammation protect pollution-induced devastating diseases. article, I discuss key findings numerous recent preclinical studies documenting first, role pollutant PM2.5 augmentation stress, associated diseases; second, efficacies different natural synthetic compounds amelioration PM2.5-induced pyroptosis, pathologies.

Язык: Английский

Процитировано

2
Air-pollutant particulate matter 2.5 (PM2.5)-induced inflammation and oxidative stress in diseases: Possible therapeutic approaches DOI Creative Commons
Asish K. Ghosh

International Journal of Science and Research Archive, Год журнала: 2024, Номер 11(1), С. 2148 - 2162

Опубликована: Фев. 18, 2024

Today, air pollution is one of the greatest threats to organismal healthspan. The environmental earth contaminated with a wide variety artificially generated pollutants like fine particulate matter (PM2.5) emitting from industry, fuel engine vehicles, biomass combustion, fumes blasting, crop residue burning, and wildfire. pollutant PM2.5 induces massive oxidative stress inflammation, major contributors in initiation progression numerous diseases including pulmonary, cardiovascular, renal, hepatic, reproductive, neurological, mental, accelerated biological aging. provocative question following: how can we solve this associated problem? As it not realistic clean environment at once toxic pollution, initiatives have been undertaken develop novel therapeutic approaches control air-pollutant-induced inflammation devastating diseases. primary goal review article discuss systematically key findings recent preclinical studies documenting first, role augmentation stress, diseases; second, efficacies different natural synthetic compounds amelioration PM2.5-induced pyroptosis, pathologies. Further investigation on safety these will be helpful select effective non-toxic compound(s) for clinical trial drug development.

Язык: Английский

Процитировано

0