Through an antioxidant mechanism, baicalein promotes remyelination and ameliorates motor dysfunction and cognitive impairment in an animal model of multiple sclerosis.

Abstract

The hallmark deficits of multiple sclerosis (MS), a chronic inflammatory and
neurodegenerative disease, are caused by recurrent demyelination that destroys remyelination and disrupts
axonal conduction. Traditional Chinese medicines are becoming more and more popular as researchers look
for new medications to treat multiple sclerosis.
Techniques: In animal studies, C57BL/6J male mice were given cuprizone (CPZ), a copper chelator harmful
to cell mitochondria, to create an animal model of multiple sclerosis. By looking at how baicalein (BA)
affected the neuropathological alterations and behavioral abnormalities brought on by CPZ, the therapeutic
benefits of BA were thoroughly examined. Additionally, the molecular and cellular processes that underlie
BA's therapeutic actions were investigated. The OLN-93 cell line and cultivated oligodendrocyte (OL)
lineage cells were used in the in vitro tests under different CPZ, H2O2, and BA conditions. Cell biology
and biochemical techniques were used to assess the cultivated cells' survival, development, and
mitochondrial activity as well as any oxidative stress indicators.
Findings: In the in vivo tests, BA promoted the remyelination process and reduced neuroinflammation in
the brains of CPZ-exposed mice, aiding in the recovery of their motor and cognitive deficits. Underpinning
these protective effects, BA's antioxidant activities kept the signal pathway at normal levels by preventing
the over-activation of nuclear factor erythroid 2-related factor 2 (NRF2) and its downstream antioxidant
enzymes (HO-1, NQO1, and SOD2). The in vitro tests demonstrated that CPZ and H2O2 both cause
oxidative stress and damage to the cell's mitochondria, which delays the formation of oligodendrocyte (OL)
lineage cells. By scavenging ROS produced by the cells' damaged mitochondria, BA successfully stopped
the development delay of cultivated OLs.