4.7 Article

Noise-Induced Vascular Dysfunction, Oxidative Stress, and Inflammation Are Improved by Pharmacological Modulation of the NRF2/HO-1 Axis

期刊

ANTIOXIDANTS
卷 10, 期 4, 页码 -

出版社

MDPI
DOI: 10.3390/antiox10040625

关键词

environmental risk factors; aircraft noise exposure; inflammation; endothelial dysfunction; oxidative stress; heme oxygenase-1; NRF2

资金

  1. Boehringer Ingelheim Foundation

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This study investigated the protective effects of HO-1 inducer and NRF2 activator on mice exposed to aircraft noise, showing that these treatments can mitigate the adverse effects of noise on vascular function by normalizing arterial hypertension and vascular dysfunction, as well as reducing oxidative stress and inflammation levels triggered by noise exposure. The study identifies new potential targets for mitigating the health effects of environmental noise exposure, suggesting that natural dietary constituents with HO-1 and NRF2 induction properties could be promising for preventive measures.
Vascular oxidative stress, inflammation, and subsequent endothelial dysfunction are consequences of traditional cardiovascular risk factors, all of which contribute to cardiovascular disease. Environmental stressors, such as traffic noise and air pollution, may also facilitate the development and progression of cardiovascular and metabolic diseases. In our previous studies, we investigated the influence of aircraft noise exposure on molecular mechanisms, identifying oxidative stress and inflammation as central players in mediating vascular function. The present study investigates the role of heme oxygenase-1 (HO-1) as an antioxidant response preventing vascular consequences following exposure to aircraft noise. C57BL/6J mice were treated with the HO-1 inducer hemin (25 mg/kg i.p.) or the NRF2 activator dimethyl fumarate (DMF, 20 mg/kg p.o.). During therapy, the animals were exposed to noise at a maximum sound pressure level of 85 dB(A) and a mean sound pressure level of 72 dB(A). Our data showed a marked protective effect of both treatments on animals exposed to noise for 4 days by normalization of arterial hypertension and vascular dysfunction in the noise-exposed groups. We observed a partial normalization of noise-triggered oxidative stress and inflammation by hemin and DMF therapy, which was associated with HO-1 induction. The present study identifies possible new targets for the mitigation of the adverse health effects caused by environmental noise exposure. Since natural dietary constituents can achieve HO-1 and NRF2 induction, these pathways represent promising targets for preventive measures.

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