Research Paper Advance Articles

Depletion of SENP1-mediated PPARγ SUMOylation exaggerates intermittent hypoxia-induced cognitive decline by aggravating microglia-mediated neuroinflammation

The effect of peroxisome proliferator-activated receptor-γ (PPARγ) on the inflammatory response and neuronal apoptosis under intermittent hypoxia (IH) condition. (A, B) The expression of PPARγ in BV-2 cells with SENP1 knockdown under IH condition was detected by western blot analysis. ***p C) The expression of IL-1β and TNF-α in BV-2 cells with SENP1 knockdown under IH condition were detected using ELISA. ***p D, E) The expression of NF-κB p65 in BV-2 cells and Bcl-2, Bax, Cleaved caspase-3 in HT-22 cells were detected by western blot analysis. **p p

Figure 3. The effect of peroxisome proliferator-activated receptor-γ (PPARγ) on the inflammatory response and neuronal apoptosis under intermittent hypoxia (IH) condition. (A, B) The expression of PPARγ in BV-2 cells with SENP1 knockdown under IH condition was detected by western blot analysis. ***p < 0.001 versus the dimethyl sulfoxide (DMSO) group. The DMSO group, BV-2 cells were pretreated with 0.1% DMSO; DMSO+GW1929 group, BV-2 cells were pretreated with 10 μM GW1929 and 0.1% DMSO; untreated BV-2 cells with SENP1 knockdown were used as the control group. (C) The expression of IL-1β and TNF-α in BV-2 cells with SENP1 knockdown under IH condition were detected using ELISA. ***p < 0.001 versus the DMSO group. (D, E) The expression of NF-κB p65 in BV-2 cells and Bcl-2, Bax, Cleaved caspase-3 in HT-22 cells were detected by western blot analysis. **p < 0.01, ***p < 0.001 versus the DMSO group or HT-22 cocultured with the medium of LV-SENP1 BV-2 cells, which added DMSO under IH condition. GW1929, a potent PPARγ agonist.