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.
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.