Poloxamer 188 Protects Isolated Adult Mouse Cardiomyocytes from Reoxygenation Injury

Abstract

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Potential Effects of Poloxamer 188 on Rat Isolated Brain Mitochondria after Oxidative Stress In Vivo and In Vitro

“…The triblock copolymer P188 has been shown to rescue a variety of tissues and cell types from I/R injury in different settings [ 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 36 , 37 , 38 ]. More recently, profound improvements in mitochondrial function through P188 after I/R injury have become apparent [ 9 , 10 , 11 , 12 , 18 , 39 , 40 ], suggesting possible direct interactions of P188 with mitochondria, specifically by stabilizing their membrane.…”

“…P188′s superb protective effects after I/R injury have been recreated in various experimental settings [ 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 36 , 37 , 38 ]. Therefore, injuring mitochondria in a way that mimics the patho-physiological processes of I/R in living cells was the premise to show any direct effects of P188 on mitochondria.…”

“…Although the triblock copolymer Poloxamer (P)188, an amphiphilic triblock copolymer, has been shown to protect different cell types, likely based on its cell-membrane-sealing effect [ 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 ], the frequently observed beneficial effect on mitochondrial function remains intriguing [ 9 , 18 ]. It is possible that the protection of cell membranes with subsequent cellular recovery generally leads to better preserved mitochondrial function as an indirect, downstream consequence.…”

Evaluation of In Vitro Neuronal Protection by Postconditioning with Poloxamer 188 Following Simulated Traumatic Brain Injury

“…To optimize the H/R ± compression protocol with mouse neurons, a series of experiments to injure the neurons were performed. We evaluated 2.5, 5 and 10 h of hypoxia ± compression, followed by 2 h of reperfusion as successfully accomplished before [ 32 ]. In this context, we were able to demonstrate that 5 h hypoxia ± compression with subsequent 2 h of reoxygenation works as a suitable in vitro mouse neuron TBI model for testing novel treatments [ 31 ].…”

“…Furthermore, the selected concentrations have been established in previous studies investigating P188. For example, P188 in concentrations ranging from 10 µM to 1 mM, administered during reoxygenation, protected mouse cardiomyocytes from I/R injury assessed by cell number/viability, LDH release, FM1-43 incorporation, Caspase 3 activity and intracellular Ca 2+ [ 32 ]. The effect of P188 has also been tested on murine myoblast cell membrane protection after exposure to hypotonic stress and isotonic recovery followed by evaluation of membrane integrity via LDH release.…”