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. 2022 Nov 22;119(3):867–878. doi: 10.1093/cvr/cvac173

Figure 2.

Figure 2

Nicotine induces and augments pro-inflammatory cytokines and ROS in human AoSMC and murine RAW264.7 cells. (A) Nicotine increases expression levels of inflammatory genes (Ccl2, Il6 and Tnf) in murine RAW264.7 cells. (B) Nicotine dose-dependently augments inflammatory gene (Ccl2, Tnf) responses to recombinant IL-6 treatment (20 ng/mL) in RAW264.7 cells. (C) Nicotine dose-dependently increases total ROS in RAW264.7 cells (DCFDA Assay, Ex/Em = 485/535 nm), a process reversed by TEMPOL. (D) Nicotine dose-dependently increases expression levels of inflammatory genes (CCL2, IL6 and IL8) in human AoSMCs. (E) Nicotine dose-dependently augments inflammatory gene (CCL2, IL6 and IL8) responses to recombinant IL-6 treatment (20 ng/mL) in human AoSMCs. (F) Nicotine dose-dependently increases ROS response to IL6 (20 ng/mL) in human AoSMCs (Abcam/Rhodamine, Ex/Em = 550/620 nm). (G) Corresponding pictures to (F) of human AoSMCs stained for ROS under green channel using ROS Detection Assay (Abcam/Rhodamine). Gene expression data are qRT–PCR presented as fold change vs. control. §P < 0.05 vs. control; vs. §§ control and IL6; † vs. control, IL6, and IL6 + nicotine 10 nM (A, B, D, and E). *P < 0.05 vs. control; #P < 0.05 vs. other group (C). *P < 0.05 or **P < 0.01 vs. IL6, #P < 0.05 vs. other group (F). All two-tailed Student’s t-test. Data are mean ± SEM (n = 4–6/treatment group).