Figure 5.

IgG functions to eliminate ROS production in response to CSF1 stimuli (A, B) Western blot and quantification show that on exposure to CSF1 stimuli, IgG levels significantly decreased about one-fold. NMN supplement significantly raised the IgG level close to the control level. (C, D) ROS live fluorescence shows that on exposure to CSF1 stimuli, ROS significantly decreased by about 40.1% on exposure to NMN supplement, ROS significantly decreased over one-fold on exposure to H2O2 stimuli, ROS significantly increased by more than one-fold. CSF1 co-supplement with NMN raised the ROS level in NMN-treated oocytes to close to the control level CSF1 co-supplement with H2O2 reduced the ROS level in H2O2-treated oocytes to near the control level. (E) Model hypothesis for (A–D) CSF1-induced IgG increment might be used to eliminate ROS production on exposure to either CSF1 or H2O2 treatment. (F, G) ROS live fluorescence shows that on exposure to CSF1 stimuli, ROS significantly decreased by about 53.7% while IgG co-inhibition significantly raised the ROS level close to the control level. On exposure to H2O2 stimuli, ROS significantly increased by more than one-fold the CSF1 co-supplement reduced the ROS level in H2O2-treated oocytes to close to the control, whereas IgG inhibition+CSF1+H2O2 significantly increased the ROS level compared with the CSF1+H2O2 group. (H) Model hypothesis for A-G: CSF1 treatment could induce both IgG and ROS increment increased IgG can be used to counteract the increment of ROS on exposure to CSF1 or H2O2 stimuli. (I-K) Western blot and quantification show that SOD2 significantly increased in response to CSF1, while decreased upon IgG inhibition or CSF1 treatment plus IgG inhibition GPX4 level was not affected by CSF1 treatment but decreased upon IgG inhibition. Actin was used as a loading control. Scale bars, 20 μm. Difference lower-case letters indicate significant difference between two groups.