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Sulforaphane protects MLE-12 lung epithelial cells against oxidative damage caused by ambient air particulate matter

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Abstract

Ambient air particulate matter with aerodynamic diameters ≤2.5 μm (PM2.5) can cause pulmonary injury. Oxidative stress is thought to be an important mechanism of PM2.5-mediated toxicity. Sulforaphane (SFN), a compound derived from cruciferous vegetables, is a well-known potent antioxidant; however, its protective effect on lung epithelial cells exposed to PM2.5 is unclear. The results showed that SFN pre-treatment markedly inhibited PM2.5-induced apoptosis of the type II alveolar epithelial cell line MLE-12 by elevating glutathione S-transferase levels and decreasing reactive oxygen species. SFN pre-treatment down-regulated the expression of the pro-apoptotic proteins Bax and Bad, and reduced the activity of caspase-3, while it up-regulated the expression of the anti-apoptotic protein Bcl-2. Moreover, SFN induced the activation of the Akt and ERK pathways, and up-regulated the expression of Nrf2 and its downstream antioxidant genes NQO-1 and HO-1. This is the first study to demonstrate that SFN could protect MLE-12 cells against PM2.5-induced oxidative damage via activation of the Nrf2 pathway and inhibition of the mitochondrial apoptotic pathway; therefore, SFN may be a promising compound for preventing PM2.5-triggered pulmonary cell damage.

Graphical abstract: Sulforaphane protects MLE-12 lung epithelial cells against oxidative damage caused by ambient air particulate matter

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Publication details

The article was received on 30 Jun 2017, accepted on 16 Oct 2017 and first published on 07 Nov 2017


Article type: Paper
DOI: 10.1039/C7FO00969K
Citation: Food Funct., 2017, Advance Article
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    Sulforaphane protects MLE-12 lung epithelial cells against oxidative damage caused by ambient air particulate matter

    A. Wang, Y. Xu, Z. Zhang, B. Lu, X. Yin, A. Yao, L. Han, Z. Zou, Z. Li and X. Zhang, Food Funct., 2017, Advance Article , DOI: 10.1039/C7FO00969K

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