HB-EGF Ameliorates Oxidative Stress-Mediated Uterine Decidualization Damage

Figure 7

Effects of HB-EGF on mitochondrial O₂⁻ and mitochondrial respiratory chain complex under oxidative stress. (a–c) Effects of HB-EGF on the activities of mitochondrial respiratory chain complex I, II, and III in stromal cells under oxidative stress. (d and e) NAC reduced the mitochondrial O₂⁻ in stromal cells after exposure to H₂O₂. (d and f) Mitochondrial respiratory chain complex I and III mediated the effects of HB-EGF on mitochondrial O₂⁻ under oxidative stress. After treatment with ROT or AA and addition of rHB-EGF, mitochondrial O₂⁻ was analyzed by flow cytometry under oxidative stress. (g–i) Mitochondrial respiratory chain complex I and III mediated the regulation of HB-EGF on Prl8a2, Prl3c1, and ALP. After treatment with ROT or AA followed by the addition of rHB-EGF, Prl8a2 and Prl3c1 expression and ALP activity were determined.

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