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. 2022 Jul 27;27(15):4800. doi: 10.3390/molecules27154800

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© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Effect of specific inhibitor (SP600125) of JNK on PM_2.5-induced cell cycle arrest in G₀/G₁. Cells were pre-treated with hesperidin (50 µM) or with SP600125 (5 µM) for 30 min and then with PM_2.5 (50 μg/mL) for 48 h. (A) Cellular DNA was stained with propidium iodide (PI) and analyzed using flow cytometry. Cell lysates were analyzed using western blot (WB) for (B) phosphor-p53, p53, p16, (C) cyclin D1, cyclin E, Cdk2, and Cdk4 proteins. Actin was used as a loading control. * p < 0.05 compared with the control group and ^# p < 0.05 compared with the PM_2.5−treated group.

Effect of specific inhibitor (SP600125) of JNK on PM_2.5-induced cell cycle arrest in G₀/G₁. Cells were pre-treated with hesperidin (50 µM) or with SP600125 (5 µM) for 30 min and then with PM_2.5 (50 μg/mL) for 48 h. (A) Cellular DNA was stained with propidium iodide (PI) and analyzed using flow cytometry. Cell lysates were analyzed using western blot (WB) for (B) phosphor-p53, p53, p16, (C) cyclin D1, cyclin E, Cdk2, and Cdk4 proteins. Actin was used as a loading control. * p < 0.05 compared with the control group and ^# p < 0.05 compared with the PM_2.5−treated group.