Figure 1

The mortality rate, incubation rate and malformation rate after ethanol treatment. The results were analyzed by χ2 test, vs. the control group (0 μL/mL ethanol): * p < 0.05. (a) mortality rate; (b) mortality rate at 96 hpf; (c) incubation rate; (d) incubation rate at 96 hpf; (e) malformation rate; (f) malformation rate at 96 hpf.
Figure 2

The various malformation after being ethanol-treated. (a) normal; (b,c) pericardial edema, yolk sac deformity and spinal curvature; (d) pericardial edema; (e) heart bleeding; (f) liver bleeding.
Figure 3

The mortality rate (a,b) and incubation rate (c,d) after being H2O2-treated. The results were analyzed by χ2 test, vs. the control group (0 μL/mL ethanol): * p < 0.05.
Figure 4

The mortality rate (a,b) and incubation rate (c,d) after being 6-OHDA-treated (at a high concentration). The results were analyzed by χ2 test, vs. the control group (0 μL/mL ethanol): * p < 0.05.
Figure 5

The mortality rate (a,b)and incubation rate (c,d) after being 6-OHDA-treated (at a low concentration, 0–50 μmol/L). * p < 0.05.
Figure 6

Ethanol, H2O2 and 6-OHDA promote the expression of myl2a (a), selenbp1 (b) and ca2 (c). The statistical results shown represent the means (n = 3); vs. the control group (n = 3) * p < 0.05, ** p < 0.01.
Figure 7

Ethanol, H2O2 and 6-OHDA promote the expression of Nrf2b (a), sod1 (b) and sod2 (c). The statistical results shown represent the means (n = 3); vs. the control group * p < 0.05, ** p < 0.01.
Figure 8

Salvianolic acid can inhibit oxidative stress caused by ethanol. (a) The content changes of MDA increased after adding ethanol; (b) SOD activity did not change; (c) CAT activity increased; (d) GXH-Px activity decreased. The statistical results shown represent the means (n = 3); vs. the control group (n = 3) * p < 0.05, ** p < 0.01. vs. the ethanol-treated group # p < 0.05, ## p < 0.01, ### p < 0.001.
Figure 9

The expression of keap1a (a), keap1b (b), Nrf2a (c), Nrf2b (d), sod1 (e) and sod2 (f) after Sal B was added in the group of ethanol acute toxicity treatment. The statistical results shown represent the means (n = 3); vs. the control group (n = 3) * p < 0.05, ** p < 0.01, *** p < 0.001 vs. the ethanol-treated group # p < 0.05, ## p < 0.01, ### p < 0.001.
Figure 10

The expression of myl2a (a), selenbp1 (b), p53 (c) and p21 (d) after Sal B added in the group of ethanol acute toxicity treatment. The statistical results shown represent the means (n = 3); vs. the control group (n = 3) * p < 0.05, ** p < 0.01, *** p < 0.001 vs. the ethanol-treated group (n = 3) # p < 0.05, ## p < 0.01, ### p < 0.001.
Figure 11

The protein–protein interactions of oxidative-related genes.
Acknowledgments
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