Fig. 9: Summarized outcome of PUFA-plasmalogen-based LNPs and lipid-peptide (PUFA-plasmalogen-PACAP peptide) nanoassemblies-triggered CREB signaling in a Parkinson’s disease (PD) model in vitro. | Communications Chemistry

Fig. 9: Summarized outcome of PUFA-plasmalogen-based LNPs and lipid-peptide (PUFA-plasmalogen-PACAP peptide) nanoassemblies-triggered CREB signaling in a Parkinson’s disease (PD) model in vitro.

From: Sustained CREB phosphorylation by lipid-peptide liquid crystalline nanoassemblies

Fig. 9

(Left panel) The levels of phosphorylated (activated) CREB are deficient in the diseased state (a PD model generated with 6-OHDA-induced oxidative stress in 24 h-starved differentiated SH-SY5Y cells) and cannot be fully recovered by vesicular LNP administration (middle histogram PL-V in the right panel). (Right panel) Nonlamellar liquid crystalline LNPs (PL-C) induce time-dependent signal processing pathways in the PD neuronal cell response as evidenced by sustained CREB phosphorylation (right histogram PL-C). The time response to treatment by lipid-peptide nanoassemblies (PL-C + PACAP) depends on cell-penetrating properties of the studied peptide and can be enhanced with regard to stimulation by PL-V.

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