Poloxamer 188

P188 seals stable defects in cell membranes induced by skeletal muscle cell membranes rupture induced by ischemia-reperfusion injury, electroporation, irradiation, and heat damage. The full mechanism of action of P188 in inducing cytoprotective effects is not clear; however, based on in vitro experiments and the structural similarity to plasmalemma, P188 may be directly incorporated into the phospholipid bilayer to attenuate the extent of tissue injury. Its high surface activity facilitates P188 to be inserted into lipid monolayers. P188 is proposed to exert localized actions by only interacting with damaged and compromised bilayers where the local lipid packing density is reduced. In addition to the direct interaction with the membrane, P188 was shown to inhibit MMP-9 protein levels and activity, as well as the NF-κB signal pathway, in the model of acute cerebral ischemia, which is associated with increased BBB permeability leading to cerebral edema and increased penetration. MMP-9 is a key factor in extracellular matrix (ECM) degradation and BBB disruption.