Fig. 2.

ROS accumulation reduced mitochondrial membrane potential in TGEV infected PK-15 cells. (A) TGEV infection induced collapse of Δψm. Cells were infected with 10 MOI of TGEV for different times, and stained with JC-1 for 15 min at room temperature, followed by FCM analysis. The increase of Δψm-depolarized cells was that Δψm-depolarized cells in TGEV-infected cells subtracted Δψm-depolarized cells in mock-infected cells. ^∗P < 0.05, ^∗∗P < 0.01 versus 0 h. (B) Effects of ROS scavengers (NAC and PDTC) on ROS production in TGEV-infected PK-15 cells. The cells were infected with TGEV for 24 h, in the presence or absence of NAC (10 mM) or PDTC (100 μM), and the ROS production was analyzed by flow cytometry. The levels of ROS were that the fluorescence intensity in different treated-cells subtracted the fluorescence intensity in control cells. ^∗∗P < 0.01 versus TGEV infection without NAC and PDTC. (C) Effects of ROS scavengers (NAC and PDTC) on Δψm in TGEV-infected PK-15 cells. The cells were infected with TGEV for 24 h, in the presence or absence of NAC (10 mM) or PDTC (100 μM), and the Δψm were analyzed by flow cytometry. The increase of Δψm-depolarized cells was that Δψm-depolarized cells in different treatment subtracted Δψm-depolarized cells in the control. ^∗∗P < 0.01 versus TGEV infection without NAC and PDTC.