Skip to main content
. 2019 Feb 22;14(2):e0212749. doi: 10.1371/journal.pone.0212749

Fig 1. Cigarette smoke extracts and Cd increase γ-secretase-mediated NICD level.

Fig 1

(A) C6 cells were treated for 6 h with 0, 1, 10, and 25 μM Cd, lysed in RIPA buffer, and the lysates were probed with antibodies against NICD. (B) C6 cells were pretreated for 1 h with γ-secretase inhibitors (2.5 μM DAPT) followed by exposure to 25 μM Cd for 6 h. (C) C6 cells were exposed 10 and 25 μg/ml CSE, lysed, and the lysates were probed with antibodies against NICD. (D) C6 cells were pretreated for 1 h with γ-secretase inhibitors (2.5 μM DAPT) and then exposed to 25 μg /ml CSE for 6 h. β-actin was used as a loading control for lysates. (E) The effect of Cd on the viability of C6 cells was evaluated by MTT assay. Cells were pretreated for 1 h with γ-secretase inhibitors (2.5 μM DAPT) and then exposed to 25 μM Cd for 6 h. (F) Effect of CSE on the viability of C6 cells was evaluated. Cells were pretreated for 1 h with γ-secretase inhibitors (2.5 μM DAPT) and then exposed 25 μg/ml CSE. Immunoblot analysis of apoptosis-related proteins. (G) Cells were pretreated for 1 h with γ-secretase inhibitors (2.5 μM DAPT) and then exposed to 10, 25 μM Cd for 6 h. (H) Cells were pretreated for 1 h with γ-secretase inhibitors (2.5 μM DAPT) and then exposed to 10, 25 μg/ml CSE for 6 h. The lysates were probed with antibodies against c-caspase-3 (Asp175) and c-PARP (Asp214/215). β-actin was used as a loading control for lysates. Data are shown as the mean ± SD (n = 3), **P<0.01, ***P<0.001, compared to control.