Figures & data
Figure 1. Montelukast treatment increased the expression of PGC-1α in Beas-2b cells. (A–B) Beas-2b cells were stimulated with montelukast (5, 10, and 20 µM) for 24 h. Expression of PGC-1α was measured (*, p < .01 vs. vehicle group; #, p < .01 vs. 5 µM montelukast group; $, p < .01 vs. 10 µM montelukast group, n = 5–6).
![Figure 1. Montelukast treatment increased the expression of PGC-1α in Beas-2b cells. (A–B) Beas-2b cells were stimulated with montelukast (5, 10, and 20 µM) for 24 h. Expression of PGC-1α was measured (*, p < .01 vs. vehicle group; #, p < .01 vs. 5 µM montelukast group; $, p < .01 vs. 10 µM montelukast group, n = 5–6).](/cms/asset/d6cd1af4-b0e0-44d2-90c0-bb3a1d0b4327/ianb_a_1687502_f0001_b.jpg)
Figure 2. Montelukast treatment increased the expression of NRF-1 and TFAM in Beas-2b cells. (A–B) Beas-2b cells were treated with 10 µM montelukast for 24 h. Expression of NRF-1 and TFAM was measured (*, p < .01 vs. vehicle group, n = 5–6).
![Figure 2. Montelukast treatment increased the expression of NRF-1 and TFAM in Beas-2b cells. (A–B) Beas-2b cells were treated with 10 µM montelukast for 24 h. Expression of NRF-1 and TFAM was measured (*, p < .01 vs. vehicle group, n = 5–6).](/cms/asset/1a431f9a-c8db-4817-a162-0cd1f7fc73d2/ianb_a_1687502_f0002_b.jpg)
Figure 3. Montelukast treatment promoted mitochondrial biogenesis in Beas-2b cells. Cells were stimulated with 10 µM montelukast for 24 h. (A) Mitochondrial mass; (B) mtDNA/nDNA; (C) Expression of cytochrome B (*, p < .01 vs. vehicle group, n = 5–6).
![Figure 3. Montelukast treatment promoted mitochondrial biogenesis in Beas-2b cells. Cells were stimulated with 10 µM montelukast for 24 h. (A) Mitochondrial mass; (B) mtDNA/nDNA; (C) Expression of cytochrome B (*, p < .01 vs. vehicle group, n = 5–6).](/cms/asset/c1610dea-1409-4724-ad8b-f2c4bd22b898/ianb_a_1687502_f0003_c.jpg)
Figure 4. Montelukast treatment induced a gain in mitochondrial function in Beas-2b cells. Cells were stimulated with 10 µM montelukast for 24 h. (A). Representative results of oxygen content consumption in non-treated (blue curve) and montelukast-treated (purple curve) Beas-2b cells; (B). Summarized mitochondrial respiratory rate (*, p < .01 vs. vehicle group, n = 6).
![Figure 4. Montelukast treatment induced a gain in mitochondrial function in Beas-2b cells. Cells were stimulated with 10 µM montelukast for 24 h. (A). Representative results of oxygen content consumption in non-treated (blue curve) and montelukast-treated (purple curve) Beas-2b cells; (B). Summarized mitochondrial respiratory rate (*, p < .01 vs. vehicle group, n = 6).](/cms/asset/56df5a39-a965-4413-8f66-5b605a18f6d0/ianb_a_1687502_f0004_c.jpg)
Figure 5. Montelukast treatment increased the production of ATP in Beas-2b cells. Cells were stimulated with 10 µM montelukast for 24 h. ATP production was measured (*, p < .01 vs. vehicle group, n = 6).
![Figure 5. Montelukast treatment increased the production of ATP in Beas-2b cells. Cells were stimulated with 10 µM montelukast for 24 h. ATP production was measured (*, p < .01 vs. vehicle group, n = 6).](/cms/asset/d8dbdc2f-64ec-4855-b440-dc150c29eee4/ianb_a_1687502_f0005_b.jpg)
Figure 6. Montelukast-induced generation of cAMP in Beas-2b cells. Cells were stimulated with 10 µM montelukast for 1 h. Intracellular levels of cAMP were determined (*, p < .01 vs. vehicle group, n = 6).
![Figure 6. Montelukast-induced generation of cAMP in Beas-2b cells. Cells were stimulated with 10 µM montelukast for 1 h. Intracellular levels of cAMP were determined (*, p < .01 vs. vehicle group, n = 6).](/cms/asset/47de0fb4-3371-4cd7-bd13-82072ae99989/ianb_a_1687502_f0006_b.jpg)
Figure 7. Montelukast-induced expression of PGC-1α in Beas-2b cells is mediated by cAMP/CREB. (A) Beas-2b cells were stimulated with 10 µM montelukast for 1 h. Phosphorylated and total levels of CREB were determined; (B) Cells were stimulated with 10 µM montelukast with or without H89 (10 μM) for 24 h. The expressions of phosphorylated CREB, total CREB and PGC-1α were measured by western blot analysis; (C) Beas-2b cells were stimulated with 10 µM montelukast with or without H89 (10 μM) for 24 h. The expressions of NRF1 and TFAM were measured by western blot analysis; (D) Beas-2b cells were stimulated with 10 µM montelukast with or without H89 (10 μM) for 24 h. mtDNA/nDNA was determined (*, #, p < .01 vs. previous column group, n = 6).
![Figure 7. Montelukast-induced expression of PGC-1α in Beas-2b cells is mediated by cAMP/CREB. (A) Beas-2b cells were stimulated with 10 µM montelukast for 1 h. Phosphorylated and total levels of CREB were determined; (B) Cells were stimulated with 10 µM montelukast with or without H89 (10 μM) for 24 h. The expressions of phosphorylated CREB, total CREB and PGC-1α were measured by western blot analysis; (C) Beas-2b cells were stimulated with 10 µM montelukast with or without H89 (10 μM) for 24 h. The expressions of NRF1 and TFAM were measured by western blot analysis; (D) Beas-2b cells were stimulated with 10 µM montelukast with or without H89 (10 μM) for 24 h. mtDNA/nDNA was determined (*, #, p < .01 vs. previous column group, n = 6).](/cms/asset/d3b08286-6a51-42fa-bece-5749a50446b5/ianb_a_1687502_f0007_b.jpg)