Neuroprotective Effect of Didymin on Hydrogen Peroxide-Induced Injury in the Neuronal Membrane System

Abstract

In this study, the flavonoid didymin was administered in vitro in neuronal cells after hydrogen peroxide (H₂O₂)-induced injury (neurorescue) in order to investigate the effects of this natural molecule on cell damage in a neuronal membrane system. The results showed the effects of didymin in neuronal cells by using a polycaprolactone biodegradable membrane system as an in vitro model. Two major findings are presented in this study: first is the antioxidant property of didymin and, second, for the first time we provide evidence concerning its ability to rescue neuronal cells from oxidative damage. Didymin showed radical scavenging activities and it protected the neuronal cells against H₂O₂-induced neurotoxicity. Didymin increased cell viability, decreased intracellular reactive oxygen species generation, stimulated superoxide dismutase, catalase and glutathione peroxidase activity in neuronal cells which were previously insulted with H₂O₂. In addition, didymin strikingly inhibited H₂O₂-induced mitochondrial dysfunctions in terms of reduction of mitochondria membrane potential and the activation of cleaved caspase-3, and also decreased dramatically the H₂O₂-induced phosphorylation of c-Jun N-terminal kinase. Therefore, this molecule is capable of inducing recovery from oxidative damage, and promoting and/or restoring normal cellular conditions. Moreover, the mechanism underlying the protective effects of didymin in H₂O₂-injured neuronal cells might be related to the activation of antioxidant defense enzymes as well as to the inhibition of apoptotic features, such as p-JNK and caspase-3 activation. These data suggest that didymin may be a potential therapeutic molecule for the treatment of neurodegenerative disorders associated with oxidative stress.

Neuronal Differentiation Modulated by Polymeric Membrane Properties

“…On PLGA, PLGA/Col1, CHT/Col10, CHT/Col30, and CHT/Col50 membranes, cells acquired a neuron-like phenotype that was characterized by spindle-like cell somata with extensive neurite outgrowth and rich arborization. This neuron-like morphology is similar to that described in our previous works [Morelli et al, 2014[Morelli et al, , 2015a[Morelli et al, , 2017 and by others [Cheung et al, 2009]. The different neuronal response could be attributed to the improved mechanical properties and the moderate hydrophilic surface of the collagen-blend polymeric membranes.…”

Neurotoxic Agent-Induced Injury in Neurodegenerative Disease Model: Focus on Involvement of Glutamate Receptors

“…Cell lines, including BV-2 microglia, PC12 cells, and SH-SY5Y cells, are ideal for studying H 2 O 2 -induced neurotoxicity. In experimental models, H 2 O 2 -induced neurotoxicity causes mitochondrial dysfunction, oxidative stress, cytotoxicity, apoptosis, and neuronal cell death (Han et al, 2014; Morelli et al, 2014; Ismail et al, 2015; Mesbah-Ardakani et al, 2016; Zhong et al, 2016; Masilamani et al, 2017; Oh et al, 2017) while it also modulates glutamate receptors. Exposure to H 2 O 2 can activate normally silent NMDARs, potentially via the inhibition of redox-sensitive glutamate uptake.…”

Polymeric membranes modulate human keratinocyte differentiation in specific epidermal layers

“…The degradation properties of the membranes were investigated by treatment with an enzymatic solution, by using 1 mg/mL of lysozyme in PBS, as previously reported [22]. In particular, samples of 1.5x1.5 cm 2 were precisely weighed, immersed in the enzymatic solution and incubated at 37°C, with refreshing media every 7 days.…”