Nano-hesperetin enhances the functional recovery and endogenous remyelination of the optic pathway in focal demyelination model

Baradaran, Saeideh; Ghasemi-Kasman, Maryam; Moghaddam, Akbar Hajizadeh

doi:10.1016/j.brainresbull.2020.09.006

Cited by 10 publications

(1 citation statement)

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“…The mechanisms underlying the effects of CH38 could be related to anti-inflammatory and anti-oxidant properties described for flavonoids of this chemical group (Jäger & Saaby, 2011;Karabin et al, 2015;Sun et al, 2017) that ameliorated white matter damage in cuprizone (Hashimoto et al, 2017) or lysolecithin demyelinating models (Baradaran et al, 2018(Baradaran et al, , 2020. Modified flavonoids could even accelerated oligodendrocyte differentiation improving the remyelination capacity in an in vitro model of perinatal white matter injury (Su et al, 2020).…”

Section: Oligodendrocyte Ultrastructure Was the Most Affected In Ga C...mentioning

confidence: 99%

Morphological evidence of the protective effects of a synthetic chalcone against the striatal myelin damage induced by glutaric acid

Casanova

Rosillo

Jiménez

et al. 2023

Intl J of Devlp Neuroscience

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Ultrastructural features of striatal white matter and cells in an in vivo model of glutaric acidemia type I created by intracerebral injection of glutaric acid (GA) were analyzed by transmission electron microscopy and immunohistochemistry. To test if the white matter damage observed in this model could be prevented, we administered the synthetic chemopreventive molecule CH38 ((E)‐3‐(4‐methylthiophenyl)‐1‐phenyl‐2‐propen‐1‐one) to newborn rats, previous to an intracerebroventricular injection of GA. The study was done when striatal myelination was incipient and when it was already established (at 12 and 45 days post‐injection [DPI], respectively). Results obtained indicate that that the ultrastructure of astrocytes and neurons did not appear significantly affected by the GA bolus. Instead, in oligodendrocytes, the most prominent GA‐dependent injury defects included endoplasmic reticulum (ER) stress and nuclear envelope swelling at 12 DPI. Altered and reduced immunoreactivities against heavy neurofilament (NF), proteolipid protein (PLP), and myelin‐associated glycoprotein (MAG) together with axonal bundle fragmentation and decreased myelin were also found at both ages analyzed. CH38 by itself did not affect striatal cells or axonal packages. However, the group of rats that received CH38 before GA did not show evidence neither of ER stress nor nuclear envelope dilation in oligodendrocytes, and axonal bundles appeared less fragmented. In this group, labeling of NF and PLP was similar to the controls. These results suggest that the CH38 molecule is a candidate drug to prevent or decrease the neural damage elicited by a pathological increase of GA in the brain. Optimization of the treatments and identification of the mechanisms underlying CH38 protective effects will open new therapeutic windows to protect myelin, which is a vulnerable target of numerous nervous system diseases.

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