Research suggests that leak 188 may be useful in treating CNS disorders. This is based on the fact that it can prevent membrane toxicity caused by misfolded SOD1.

P188 also protects brain endothelial cells against mechanical trauma. In an in vitro model, it restored BBB permeability and mitigated disorganized tight junctions. It also regulated AQP4 expression and suppressed apoptosis.

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The highly amphiphilic nature of PEO and similar copolymers enables physical interactions between the polymer and membrane that impact local hydration states and shield macromolecular molecules from stress-induced membrane permeability (16-18). While these interactions are a key component of cellular protection, the lack of transcriptomic responses to both PEO and P188 implies that their protective effects are mediated by a non-transcriptional mechanism. For more details please visit bocor 188

To evaluate the specific cellular and molecular functions impacted by these two stimuli, differential expression results were used to evaluate gene-protein interaction networks via STRING analysis (46-48) and to perform gene set enrichment analyses. A visual representation of the network shows that genes effected by short-term exposure to P188 or osmotic stress are highly connected, with several distinct pathways impacted (Fig. 9A and SI Appendix, Table S5).

This study provides a first-time glimpse into the non-transcriptional mechanisms that allow Poloxin to provide such effective protection. Furthermore, it illustrates how the osmotic and mechanical properties of PEO and P188 are distinct from each other, yet are able to protect cells from a variety of perturbations.