The Toxicity of Cooking Oil Fumes on Human Bronchial Epithelial Cells Through ROS-Mediated MAPK, NF-κB Signaling Pathways and NLRP3 Inflammasome

Abstract Cooking oil fumes (COFs) are main pollutants in kitchen and indoor air, which threaten human health. Exposure to COFs can cause respiratory diseases and impair pulmonary function. To investigate the toxicity of COFs on human bronchial epithelial cells (Beas-2B) and explore the underlying mechanisms, MTT assay was conducted to detect the viability of Beas-2B. Intracellular reactive oxygen species (ROS) levels and nitric oxide (NO) levels were determined with DCFH-DA assay and DAF-FM assay. The expression of genes involved in inflammation were measured with quantitative real-time PCR (qRT-PCR). The phosphorylation and the expression of proteins related to Mitogen-activated protein kinase (MAPK), NF-κB signaling pathways were measured with western blot. Our results revealed that COFs decreased Beas-2B cells viability, increased the ROS levels and NO levels in cells and induced apoptosis in Beas-2B cells. The results of qRT-PCR and western blot showed that the expression of NLRP3, p65, iNOS, IL-1β, and the factors related to oxidative stress and inflammation increased, NF-κB signaling pathway and MAPK signaling pathway were activated. This study provided some useful information to alleviate the toxicity of COFs and revealed the possible mechanism for the damage on respiratory system induced by COFs.

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Sappanone A inhibits oxidative stress, inflammation and apoptosis in cigarette smoke-induced human bronchial epithelial cells through regulating Nrf2/HO-1 and TLR4/NF-κB signaling pathways

10.21203/rs.3.rs-36518/v1 ◽

2020 ◽

Author(s):

Yan Zhang ◽

Shanshan Wang ◽

Hongli Li ◽

Xia Xu

Keyword(s):

Oxidative Stress ◽

Epithelial Cells ◽

Signaling Pathways ◽

Signaling Pathway ◽

Cigarette Smoke ◽

Bronchial Epithelial Cells ◽

Chronic Obstructive ◽

Human Bronchial Epithelial Cells ◽

Bronchial Epithelial

Abstract Chronic obstructive pulmonary disease (COPD) is a common respiratory disease associated with inflammation and oxidative stress. Sappanone A (SA) is a homoisoflavanone that has been proven to have anti-inflammatory and anti-oxidant effects. However, the role of SA in COPD remains unclear. Thus, the present study was aimed to evaluate the beneficial effect of SA on COPD in vitro. The human bronchial epithelial cells were exposed to 5% cigarette smoke extracts (CSE) to induce an in vitro model of COPD. Our results showed that SA treatment significantly attenuated the CSE-caused induction of ROS and reduction of SOD and GPx activities in 16HBE cells. In addition, SA inhibited the production of inflammatory cytokines IL-6, IFN-γ, and TNF-α in CSE-stimulated 16HBE cells. Moreover, the CSE-stimulated cell apoptosis of 16HBE cells were abrogated by SA. Furthermore, we observed that SA treatment greatly promoted the activation of Nrf2/HO-1 signaling pathway, as well as inhibited the activation of TLR4/NF-κB signaling pathway in CSE-stimulated 16HBE cells. Subsequent rescue assay revealed that the protective effects of SA on CSE-stimulated 16HBE cells were reversed by Nrf2 knockdown or TLR4 overexpression. Taken together, these findings demonstrated that SA inhibits oxidative stress, inflammation and apoptosis in CSE-induced human bronchial epithelial cells through regulating Nrf2/HO-1 and TLR4/NF-κB signaling pathways.

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