Protective effects of α‐lipoic acid on cultured human nasal fibroblasts exposed to urban particulate matter
Dong Chang Lee MD, PhD Hyunsu Choi MS Jeong‐Min Oh MS Do Hee Lee MD, a Bachelor of Medicine (B.M.) Sung Won Kim MD, PhD Soo Whan Kim MD, PhD Byung Guk Kim MD, PhD … See all authors
First published: 13 February 2019 https://doi.org/10.1002/alr.22296
Funding sources for the study: This research was supported by the Basic Science Research Program through the National Research Foundation of Korea funded by the Ministry of Education (NRF‐2017R1D1A1B03032768), the Otorhinolaryngology Alumni Fund of the Catholic University of Korea made in the program year of 2018, and a grant from the Clinical Research Institute (CMCDJ‐P‐2017‐016) funded by The Catholic University of Korea, Daejeon St Mary's Hospital.
Potential conflict of interest: None provided.
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Abstract
Background
Exposure to urban particulate matter (UPM) has been studied as a cause of various health problems. Although the association between UPM and the respiratory tract has been well studied, further research is required to characterize the effects of UPM on the upper respiratory tract. We investigated the effects of UPM‐induced reactive oxygen species (ROS) production on cultured human nasal fibroblasts, as well as the protective effects of α‐lipoic acid (ALA) on ROS production and the underlying signaling pathways involved in ROS inhibition.
Methods
Human turbinate tissue specimens were collected from 6 patients. The effects of UPM on the viability of cultured nasal fibroblasts were determined. A fluorescent malondialdehyde assay was used to measure ROS levels. Real‐time reverse transcription polymerase chain reaction was used to measure the messenger RNA levels of genes encoding Nrf2, the antioxidant response elements (AREs) (HO‐1, NQO1), and the proinflammatory cytokines (interleukin‐6 and interleukin‐8) before and after ALA treatment. Western blotting analyses were used to measure nuclear and cytosolic Nrf2 and AREs.
Results
UPM reduced cell viability and increased ROS expression in nasal fibroblasts. ALA treatment decreased ROS production in UPM‐exposed fibroblasts via the Nrf2, HO‐1, and NQO‐1 pathways. Also, ALA treatment abrogated increases in the interleukin‐6 and ‐8 levels induced by UPM in nasal fibroblasts.
Conclusion
UPM exposure resulted in increased ROS production in nasal fibroblasts. ALA treatment inhibited this increase via the Nrf2 pathway, suggesting that ALA may have a protective effect against rhinitis caused by ROS expression induced by exposure to UPM.
Dong Chang Lee MD, PhD Hyunsu Choi MS Jeong‐Min Oh MS Do Hee Lee MD, a Bachelor of Medicine (B.M.) Sung Won Kim MD, PhD Soo Whan Kim MD, PhD Byung Guk Kim MD, PhD … See all authors
First published: 13 February 2019 https://doi.org/10.1002/alr.22296
Funding sources for the study: This research was supported by the Basic Science Research Program through the National Research Foundation of Korea funded by the Ministry of Education (NRF‐2017R1D1A1B03032768), the Otorhinolaryngology Alumni Fund of the Catholic University of Korea made in the program year of 2018, and a grant from the Clinical Research Institute (CMCDJ‐P‐2017‐016) funded by The Catholic University of Korea, Daejeon St Mary's Hospital.
Potential conflict of interest: None provided.
Read the full text
ePDFPDFTOOLS SHARE
Abstract
Background
Exposure to urban particulate matter (UPM) has been studied as a cause of various health problems. Although the association between UPM and the respiratory tract has been well studied, further research is required to characterize the effects of UPM on the upper respiratory tract. We investigated the effects of UPM‐induced reactive oxygen species (ROS) production on cultured human nasal fibroblasts, as well as the protective effects of α‐lipoic acid (ALA) on ROS production and the underlying signaling pathways involved in ROS inhibition.
Methods
Human turbinate tissue specimens were collected from 6 patients. The effects of UPM on the viability of cultured nasal fibroblasts were determined. A fluorescent malondialdehyde assay was used to measure ROS levels. Real‐time reverse transcription polymerase chain reaction was used to measure the messenger RNA levels of genes encoding Nrf2, the antioxidant response elements (AREs) (HO‐1, NQO1), and the proinflammatory cytokines (interleukin‐6 and interleukin‐8) before and after ALA treatment. Western blotting analyses were used to measure nuclear and cytosolic Nrf2 and AREs.
Results
UPM reduced cell viability and increased ROS expression in nasal fibroblasts. ALA treatment decreased ROS production in UPM‐exposed fibroblasts via the Nrf2, HO‐1, and NQO‐1 pathways. Also, ALA treatment abrogated increases in the interleukin‐6 and ‐8 levels induced by UPM in nasal fibroblasts.
Conclusion
UPM exposure resulted in increased ROS production in nasal fibroblasts. ALA treatment inhibited this increase via the Nrf2 pathway, suggesting that ALA may have a protective effect against rhinitis caused by ROS expression induced by exposure to UPM.
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