Research Paper Volume 13, Issue 8 pp 11363—11380

Melatonin attenuates smoking-induced atherosclerosis by activating the Nrf2 pathway via NLRP3 inflammasomes in endothelial cells

CSE induced ROS generation and upregulated NRF2 pathway in HAECs. (A, B) Cellular ROS level was measured with flow cytometry, and ROS level was promoted after CSE treatment. (C–G) Western blotting on protein level of n-Nrf2 and c-Nrf2 was performed to analyze Nrf2 nuclear translocation, suggesting that CSE increased Nrf2 nuclear translocation. The protein levels of HO-1 and NQO1 were upregulated in HAECs after treatment with CSE, as indicated by western blot results. β-Actin was used as an internal control. (H–J) The mRNA levels of Nrf2, HO-1 and NQO1 were upregulated in HAECs after treatment with CSE, as indicated by RT-PCR results. *p p ns, not significant. The data are represented as mean ± SD (n = 3).

Figure 3. CSE induced ROS generation and upregulated NRF2 pathway in HAECs. (A, B) Cellular ROS level was measured with flow cytometry, and ROS level was promoted after CSE treatment. (CG) Western blotting on protein level of n-Nrf2 and c-Nrf2 was performed to analyze Nrf2 nuclear translocation, suggesting that CSE increased Nrf2 nuclear translocation. The protein levels of HO-1 and NQO1 were upregulated in HAECs after treatment with CSE, as indicated by western blot results. β-Actin was used as an internal control. (HJ) The mRNA levels of Nrf2, HO-1 and NQO1 were upregulated in HAECs after treatment with CSE, as indicated by RT-PCR results. *p < 0.05, **p < 0.01, ns, not significant. The data are represented as mean ± SD (n = 3).