Research Paper Volume 11, Issue 19 pp 8120—8138

The interaction between STAT3 and nAChRα1 interferes with nicotine-induced atherosclerosis via Akt/mTOR signaling cascade

Figure 3. STAT3 inhibition reduces nicotine-induced inflammation in RAW264.7 cells via the Akt/mTOR/MMP2 pathway. (A) The effect of AG490 on the nicotine-induced activation of STAT3, Akt, and mTOR and the upregulation of MMP2 expression in RAW264.7 cells. (B) The effect of rapamycin on the nicotine-induced upregulation of MMP2. (C) The regulation of nicotine-induced MCP-1 expression by STAT3 and rapamycin inhibition, as detected by immunofluorescence. Magnification, 200×; bars, 100 μm. (D) ELISA was used to detect IFN-γ and IL-10 released by RAW264.7 cells upon treatment with nicotine, AG490 and rapamycin. Ni, nicotine. The data were presented as the mean ± SD. *p < 0.05, **p < 0.01 vs. the control group. #p < 0.05, ##p < 0.01 vs. the nicotine group. Each experiment was performed three times.