期刊
TOXICS
卷 9, 期 11, 页码 -出版社
MDPI
DOI: 10.3390/toxics9110276
关键词
1-nitropyrene; proinflammatory cytokines; PGE2; NF-kappa B pathway; Akt
资金
- Ministry of Science and Technology of Taiwan [MOST 109-2320-B-040-MY3]
- Chung Shan Medical University [NCHU-CSMU-10810, NCHU-CSMU-11005]
- Zuoying Branch of Kaohsiung Armed Forces General Hospital [ZBH108-07]
The study revealed that 1-NP induces a proinflammatory response through activation of the NF-kappa B pathway via Akt phosphorylation. This suggests that 1-NP triggers inflammation via the NF-kappa B pathway.
Air pollution is a major environmental and public health problem worldwide. A nitro-polycyclic aromatic hydrocarbon and the most abundant air pollutant in diesel engine exhaust, 1-nitropyrene (1-NP), is caused by the incomplete combustion of carbonaceous organic substances. Macrophages are effector cells of the innate immune cells that provide resistance in the peripheral tissue. The overactivation of macrophages results in inflammation. The generation of proinflammatory cytokines, such as interleukin (IL)-1 beta, IL-6, and tumour necrosis factor alpha, is induced by 1-NP in a concentration-dependent manner in macrophages. In this study, the production of proinflammatory mediators, such as nitrogen oxide and prostaglandin E2, was induced by 1-NP in a concentration-dependent manner through the expression of iNOS and COX2. The generation of proinflammatory cytokines, iNOS, and COX2 was induced by 1-NP through nuclear factor (NF)-kappa B p65 phosphorylation and the degradation of its upstream factor, I kappa B. Finally, Akt phosphorylation was induced by 1-NP in a concentration-dependent manner. These findings suggest that 1-NP exhibits a proinflammatory response through the NF-kappa B pathway activation due to Akt phosphorylation.
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