Ketone Bodies Mediate Antiseizure Effects

Krueger, Jena M.; Nordli, Douglas R.

doi:10.15844/pedneurbriefs-29-9-2

Cited by 3 publications

(3 citation statements)

References 4 publications

(4 reference statements)

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“…Most studies on the protective effect of apelin-13 against cerebral I/R injury have focused on the nervous system. [33][34][35][36] In this study, we used an OGD/R model, a classical model of cerebral ischemia, to test the protective effect of apelin-13 on TJs in bEnd.3 cells treated with OGD/R. Our goal was to characterize the ability of apelin-13 to attenuate disruption of the BBB following cerebral I/R injury.…”

Section: Discussionmentioning

confidence: 99%

Apelin-13 prevents the effects of oxygen–glucose deprivation/reperfusion on bEnd.3 cells by inhibiting AKT–mTOR signaling

Zhang

Cheng

et al. 2022

Exp Biol Med (Maywood)

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Autophagy plays works by degrading misfolded proteins and dysfunctional organelles and maintains intracellular homeostasis. Apelin-13 has been investigated as an agent that might protect the blood–brain barrier (BBB) from cerebral ischemia/reperfusion (I/R) injury. In this study, we examined whether apelin-13 protects cerebral microvascular endothelial cells, important components of the BBB, from I/R injury by regulating autophagy. To mimic I/R injury, the mouse cerebral microvascular endothelia l cell line bEnd 3 undergoes the process of oxygen and glucose deprivation and re feeding in the process of culture. Cell viability was detected using a commercial kit, and cell migration was monitored by in vitro scratch assay. The tight junction (TJ) proteins ZO-1 and occludin; the autophagy markers LC3 II, beclin 1, and p62; and components of the AKT–mTOR signaling pathway were detected by Western blotting and immunofluorescence. To confirm the role of autophagy in OGD/R and the protective effect of apelin-13, we treated the cells with 3-methyladenine (3-MA), a pharmacological inhibitor of autophagy. Our results demonstrated that OGD/R increased autophagic activity but decreased viability, abundance of TJs, and migration. Viability and TJ abundance were further reduced when the OGD/R group was treated with 3-MA. These results indicated that bEnd.3 upregulates autophagy to ameliorate the effects of OGD/R injury on viability and TJs, but that the autophagy induced by OGD/R alone is not sufficient to protect against the effect on cell migration. Treatment of OGD/R samples with apelin-13 markedly increased viability, TJ abundance, and migration, as well as autophagic activity, whereas 3-MA inhibited this increase, suggesting that apelin-13 exerted its protective effects by upregulating autophagy.

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Section: Discussionmentioning

confidence: 99%

Apelin-13 prevents the effects of oxygen–glucose deprivation/reperfusion on bEnd.3 cells by inhibiting AKT–mTOR signaling

Zhang

Cheng

et al. 2022

Exp Biol Med (Maywood)

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“…Contributing Editors provide detailed summaries of published articles, followed by commentaries based on their experience and corroborated by appropriate supplementary citations. The two most highly accessed articles published in 2015 covered topics related to epilepsy including the mechanisms of the ketogenic diet [ 5 ] and the history of the specific EEG term, “hypsarhythmia” [ 6 ].…”

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confidence: 99%

The 30-Year Anniversary of Pediatric Neurology Briefs

Jj¹,

2016

Pediatr Neurol Briefs

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“…Further studies comparing metabolic changes in ketogenic diet responders and nonresponders and significance of amino acid and pterin variations are indicated. Recent articles regarding the mechanism of action of the diet (previously reviewed in Pediatric Neurology Briefs ) reemphasize the importance of ketone bodies as a factor [ 5 ], and introduce a novel mechanism and potential treatment with LDH inhibitors [ 6 ].…”

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confidence: 99%