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

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Figure 1.

Intermittent hypoxia (IH) triggers inflammatory response, neuronal apoptosis and the SUMOylation of peroxisome proliferator-activated receptor-γ (PPARγ). (A) The expression of IL-1β and TNF-α in BV-2 cells under normoxic and IH conditions were detected using ELISA. ***p < 0.001 versus the normoxia group. (B, C) 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 normoxia group. (D, E) The effects of IH on the SUMOylation of PPARγ and the level of PPARγ (D, F) were detected by co-immunoprecipitation followed by western blot analysis. ***p < 0.001 versus the normoxia group. NF-κB p65, nuclear factor kappa B p65. Bcl-2, Bax, Cleaved caspase-3 are apoptosis-related proteins. IL-1β, interleukin-1β; TNF-α, tumor necrosis factor-α. Normoxia: BV-2 cells were cultured in normoxic condition. IH: BV-2 cells were exposed to IH. SUMO, small ubiquitin-like modifier; ELISA, enzyme-linked immunosorbent assay; IP, immunoprecipitation; IB, immunoblot.