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. Author manuscript; available in PMC: 2019 Jun 21.
Published in final edited form as: Free Radic Biol Med. 2019 Feb 18;134:630–643. doi: 10.1016/j.freeradbiomed.2019.02.015

Fig. 5. Treatment with a G9a inhibitor, UNC0638 reduced the induction of H3K9Me2, and transcriptional activation of Nrf2 following TBI.

Fig. 5

(A) Confocal microscopic analysis shows that the induction of H3K9Me2 in RGC was decreased after treatment with UNC0638 following TBI. (B) Confocal microscopic examination shows that the induction of H3K9Me2 in the optic nerve was reduced after treatment with UNC0638 following TBI. (C–F) the quantitative RT-PCR analysis shows that the decrease in mRNA level of sod (C, E) and catalase (D, F) either in the retina or optic nerve was rescued in TBI-mice treated with UNC0638. (G–H) The ChIP assay suggests that a decrease in Nrf2 binding to the sod promoter was attenuated in the retina (G) and optic nerve (H) in TBI-mice treated with UNC0638. (I–J) The co-immunoprecipitation (Co-IP) study shows that treatment with UNC0638 decreases the interaction between Nrf2 and H3K9Me2 after TBI in the retina (I) and optic nerve (J).