Sesamin Ameliorates Fine Particulate Matter (PM_2.5)-Induced Lung Injury via Suppression of Apoptosis and Autophagy in Rats

Abstract

Lung damage can be caused by fine particulate matter (PM2.5). Thus, effective prevention strategies for PM2.5-induced lung injury are urgently required. Sesamin (Ses) is a natural polyphenolic compound that has attracted considerable attention of researchers because of its wide range of pharmacological activities. The present study aims to elucidate whether Ses pretreatment could alleviate PM2.5-induced lung damage and identify its possible mechanisms. Sprague–Dawley rats were orally dosed with 0.5% carboxymethylcellulose (CMC) and different concentrations of Ses once a day for 21 days. Then, the rats of the PM2.5 exposure group and Ses-treated group were exposed to PM2.5 by intratracheal instillation every 2 days for 1 week. Biomarkers associated with lung injury were detected in bronchoalveolar lavage fluid (BALF). Lung tissue was collected for histology, inflammation, oxidative stress, immunohistochemistry, and Western blot. Our results showed that PM2.5 exposure could cause pathological changes in lung tissue and increase levels of TP, AKP, and ALB in BALF. Meanwhile, exposure to PM2.5 can cause oxidative stress and inflammation in the lungs. In addition, Ses pretreatment could ameliorate histopathological injury, oxidative stress, and inflammation caused by PM2.5 exposure. It could also inhibit PM2.5-induced apoptosis and upregulation of autophagy-associated proteins. Collectively, our study indicated that Ses pretreatment could ameliorate PM2.5-induced lung damage via inhibiting apoptosis and autophagy in rats.

Astaxanthin alleviates fine particulate matter (PM2.5)-induced lung injury in rats by suppressing ferroptosis and apoptosis

“…38 TNF-α and IL-6 can promote the recruitment of monocytes and white blood cells, with a significant pro-inflammatory effect. 39 According to previous studies, TNF-α, IL-1β, and IL-6 expression levels were significantly increased in rat lung tissue after exposure to PM 2.5 , 12,40 which is consistent with our findings. Our research reveals that PM 2.5 exposure significantly increased macrophage infiltration and inflammatory cytokine expression.…”

“…Previous studies have demonstrated that multiple ways of cell damage, including oxidative stress, inflammation, autophagy, necrosis, ferroptosis, and apoptosis, are associated with PM 2.5 -induced lung damage and co-existence or crosstalk. 12,27–29 However, the complex pathogenesis also gives us more ideas for mitigating the lung damage caused by PM 2.5 . The preventive intervention of natural phytochemicals is a research idea with far-reaching significance to alleviate the body damage caused by PM 2.5 .…”

“…Studies have revealed that PM 2.5 exposure can cause lung damage by inducing apoptosis in rat lung tissue cells. 12,54 According to Piao et al, PM 2.5 -induced ROS can activate the ER stress-CHOP apoptotic signal, and inhibiting the ER stress-CHOP apoptotic signal does reduce PM 2.5induced apoptosis. 55 Bcl-2 and Bax, the two signature molecules of apoptosis, are often used to reflect the apoptosis level.…”

“…10 After triggering inflammatory responses and oxidative damage, PM 2.5 can further contribute to lung remodeling and respiratory diseases, which may be primarily related to lung cell death. 11,12 It is reported that PM 2.5 can cause cell death via various mechanisms, including apoptosis, autophagy, pyroptosis, necrosis, and ferroptosis. 13 Several studies have also linked ferroptosis and apoptosis to develop lung injury.…”

MicroRNA miR-212-5p Regulates the MEK/ERK Signaling Pathway by Targeting A-Raf proto-oncogene serine/threonine-protein kinase (ARAF) to Regulate Cowshed PM2.5-Induced NR8383 Apoptosis

“…Studies have shown that PM 2.5 exposure can cause a variety of respiratory diseases, such as inflammation of airways and lung macrophages, pulmonary fibrosis, etc. [4][5][6]. At the same time, it may cause pyroptosis and ferroptosis, which can lead to pulmonary toxicity [7], particularly in livestock housing due to the dense Toxics 2023, 11, 981 2 of 17 and relatively enclosed animal population.…”