Fig. 6.

Adipocyte-derived CTRP3 activated Nrf2 to prevent oxidative stress and cell apoptosis. (A) CTRP3 expression in the pooled adipocyte medium. 3T3-L1 adipocytes were treated melatonin (10 μmol/L) or vehicle for 24 h, after which the medium was collected to detect CTRP3 expression. ConM-V: conditioned medium in which adipocytes treated with vehicle were cultured; ConM-M: conditioned medium in which adipocytes treated with melatonin were cultured. (B-C) Nrf2, HO-1 and SOD2 expression in H9c2 cells. H9c2 cells were exposed to ConM-M for different time periods and then collected for blot detection. (D) Immunostaining of Nrf2 in H9c2 cells. H9c2 cells were exposed to ConM-V or ConM-M for 4 h and then collected for blot detection. (E-F) CTRP3 deficiency in adipocytes largely abolished the effects ConM-M on Nrf2 and HO-1 expression in H9c2 cells. (G) Cell viability in all the groups. (H) Sod2 mRNA levels in H9c2 cells. (I) DCFH-DA staining and TUNEL staining. rhCTRP3, recombinant human CTRP3. All data are expressed as the mean ± SD of six independent experiments. Differences were compared by one-way ANOVA followed by Tukey's post hoc test. *P < 0.05.