일회성 운동 중 초미세먼지(PM2.5) 과흡입이 마우스 폐의 염증 및 세포사멸 반응에 미치는 영향
Effects of Hyperventilation of Fine Particulate Matter (PM2.5) During a Single Exercise Bout on Inflammatory and Apoptotic Responses in the Mouse Lung
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PURPOSE: The purpose of this study was to investigate the effects of hyperventilation in the presence of fine particulate matter (PM2.5) on inflammatory and apoptotic responses in the lungs of mice during a single bout of aerobic exercise. METHODS: The FVB/N mice were housed in a controlled SPF room and randomly divided into four groups: control (CON, n=7), fine particulate matter exposure (PM, n=7), PM and exercise (PME, n=7), and exercise only (EX, n=7). Acute PM exposure and/or aerobic treadmill exercise were undertaken according to the groups using a specially designed PM treadmill chamber. RESULTS: Protein expression and phosphorylation of p65 NF-kB in mouse lungs were significantly increased by acute exercise, but not by PM exposure. Basal protein levels and phosphorylation of MAPKs (p38, ERK, and JNK) were significantly increased in the PME group, but were lower in the PM and EX groups. Although the percentage of collagen fibers in lung tissue was not affected by PM exposure, the expression of pro- and antiapoptotic factors BAX, BID, and Bcl-2 was significantly elevated by inhalation of PM during exercise. CONCLUSIONS: In this study, the MAPKs family was activated by excessive PM inhalation during exercise and similar changes in apoptosis-related signaling were observed. This suggests that even a single bout of inhalation of fine particulate matter during exercise can affect factors associated with inflammation and cell death.
Abstract
PURPOSE: The purpose of this study was to investigate the effects of hyperventilation in the presence of fine particulate matter (PM2.5) on inflammatory and apoptotic responses in the lungs of mice during a single bout of aerobic exercise. METHODS: The FVB/N mice were housed in a controlled SPF room and randomly divided into four groups: control (CON, n=7), fine particulate matter exposure (PM, n=7), PM and exercise (PME, n=7), and exercise only (EX, n=7). Acute PM exposure and/or aerobic treadmill exercise were undertaken according to the groups using a specially designed PM treadmill chamber. RESULTS: Protein expression and phosphorylation of p65 NF-kB in mouse lungs were significantly increased by acute exercise, but not by PM exposure. Basal protein levels and phosphorylation of MAPKs (p38, ERK, and JNK) were significantly increased in the PME group, but were lower in the PM and EX groups. Although the percentage of collagen fibers in lung tissue was not affected by PM exposure, the expression of pro- and antiapoptotic factors BAX, BID, and Bcl-2 was significantly elevated by inhalation of PM during exercise. CONCLUSIONS: In this study, the MAPKs family was activated by excessive PM inhalation during exercise and similar changes in apoptosis-related signaling were observed. This suggests that even a single bout of inhalation of fine particulate matter during exercise can affect factors associated with inflammation and cell death.
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