EVNol SupraBio shows neuroprotective effects in post-ischaemic mouse brain

Published: 6-Aug-2018

Pretreatment of EVNol SupraBio shows neuroprotective effects in the cerebral ischaemia/reperfusion injury with direct effects on oxidative stress and advanced glycation end products (AGEs) reductions, and indirect effects on Nrf2 and MRP1 activations

In this interesting study, Prof. Koji Abe and his team of researchers at the Department of Neurology, Okayama University, Japan, supplemented a group of mice with EVNol SupraBio (encapsulated in a softgel capsule, branded as Tocovid) once a day for 1 month.

After 1 month of supplementation, the mice were induced for ischaemic stroke via transient middle cerebral artery occlusion (tMCAO) for 60 minutes.

The oxidative stress, apoptosis and autophagy cell death in the peri-ischaemic lesion on day 1, 3 and 7 after tMCAO in all mice were then evaluated. Two other groups of mice were used as control – one as vehicle control (treatment/supplement control) while the other act as sham control (surgery control).

Mobile activity based on Rotarod time worsened after tMCAO in the vehicle group. However, presupplementation with EVNol SupraBio resulted in significant recovery of mobile activity at day 1 after tMCAO.

Large infarcts of the lateral cortex and the underlying caudoputamen (equivalent to “dorsal striatum” in human that is a vital part of the circuitry for decision making and reward-related behaviour) were observed upon tMCAO in all groups.

What was compelling is that the infarcts volume was significantly reduced on day 1 and day 3 after tMCAO in the mice group receiving EVNol SupraBio.

The number of peroxidative damages to lipids (4-HNE), proteins (nitrotyrosine) and DNA (8-OHdG) were also significantly decreased in the EVNol SupraBio pretreatment group.

The reduced expression of AGEs biomarkers, RAGE, CMA (vascular) and CML (neuronal) in EVNol SupraBio group confirmed the neuroprotective effect of EVNol SupraBio in ischaemic mice. In addition, EVNol SupraBio pretreatment individually up-regulated Nrf2 protein level (a protein important for regulating antioxidant defense) on 7 days after tMCAO.

Under oxidative stress, GSH is rapidly oxidised to GSSG, which is toxic to the cells. It was observed that GSSG level significantly increased after tMCAO, resulting in higher GSSG/GSH ratio.

In this study, the group of mice receiving EVNol SupraBio showed an increase in MRP1 level and reduced GSSG/GSH ratio, suggesting that EVNol SupraBio protects against the damage caused by ischaemic stroke by inducing MRP1.

Supplementation with EVNol SupraBio also significantly reduced cleaved caspase-3 and LC3-II expressions, which both play an important role in autophagy and apoptosis of cell.

The researcher concluded that EVNol SupraBio pretreatment obviously has neuroprotective activities against oxidative stress, and at least in part by antiapoptotic/autophagic cell death in ischaemic mice brain.

“The neuroprotective activities of EVNol SupraBio on pre-stroke and post-stroke settings have been reported in various in vitro and clinical studies, conducted at the Ohio State University (OSU) Wexner Medical Center (funded by the US NIH) and University Science Malaysia."

“I’m pleased to see more research in EVNol SupraBio for brain protection and cognitive health. It started from OSU almost 20 years ago and it is now particularly studied in other countries such as Malaysia and Japan. These research are important as they scientifically substantiate the neuroprotective activity of EVNol SupraBio,” add Bryan See, Business Development Manager at ExcelVite.

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