Fig. 5

Overexpression of ERβ in the amygdala restores prenatal levonorgestrel exposure-induced ROS generation and DNA damage, along with dysfunction of mitochondria and fatty acid metabolism in 10-week-old offspring, while ERβ knockdown mimics the effect. The 8-week-old male offspring from the VEH group received either empty control (VEH/EMP) or ERβ knockdown (VEH/shERβ) lentivirus infusion, and the male offspring from the LNG group received either empty control (LNG/EMP) or ERβ expression (LNG/↑ERβ) lentivirus infusion, and the offspring were sacrificed at 10 weeks of age. a–l The amygdala tissues were isolated from 10-week-old treated male offspring for further analysis. a The mRNA levels for gene expression, n = 4. b The quantitation of protein levels, n = 5. c Representative bands for western blots. d SOD2 activity, n = 5. e In vivo superoxide anion release, n = 6. f Quantitation of 3-nitrotyrosine (3-NT) formation, n = 5. g 8-OHdG formation, n = 5. h Quantitation of γH2AX formation, n = 5. i Representative γH2AX western blotting band. j Mitochondrial DNA copies, n = 4. k Intracellular ATP levels, n = 5. l The in vivo palmitate oxidation rate, n = 5. m The amygdala neurons were isolated from 10-week-old treated male offspring for in vitro ¹⁴C–OA fatty acid uptake, n = 5. *P < 0.05 vs. VEH group; P < 0.05 vs. LNG group. Results are expressed as mean ± SEM