Research Paper Volume 13, Issue 11 pp 15240—15254

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

SENP1 depletion promotes the inflammatory response and neuronal apoptosis under intermittent hypoxia (IH) condition. (A–C) The expression of IL-1β and TNF-α in hippocampus under normoxic and IH conditions were detected by (A) qRT-PCR and (B, C) western blot analysis. **p p #p ##p ###p +/+-IH group. (D, E) The expression of NF-κB p65, Bcl-2, Bax, Cleaved caspase-3 in hippocampus were detected by western blot analysis. *p p ##p ###p +/+-IH group.

Figure 5. SENP1 depletion promotes the inflammatory response and neuronal apoptosis under intermittent hypoxia (IH) condition. (AC) The expression of IL-1β and TNF-α in hippocampus under normoxic and IH conditions were detected by (A) qRT-PCR and (B, C) western blot analysis. **p < 0.01, ***p < 0.001 versus the normoxia group. #p < 0.05, ##p < 0.01, ###p < 0.001 versus the SENP1+/+-IH group. (D, E) The expression of NF-κB p65, Bcl-2, Bax, Cleaved caspase-3 in hippocampus were detected by western blot analysis. *p < 0.05, ***p < 0.001 versus the normoxia group. ##p < 0.01, ###p < 0.001 versus the SENP1+/+-IH group.