The effect of levomepromazine on the healthy and injured developing mouse brain – An in vitro and in vivo study

Posod, Anna; Winkler, Ira; Wegleiter, K; Huber, E.; Urbanek, M; Kiechl‐Kohlendorfer, Ursula; Griesmaier, Elke

doi:10.1016/j.ibror.2020.09.003

Cited by 1 publication

(1 citation statement)

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“…It is reported that NAC has a protective effect against oxidative damage by regulating the Nrf2/HO-1 signal activated by oxidative stress [ 33 ]. As a limitation of this study, further studies are required on the signaling mechanism of Nrf2/HO-1 [ 34 ] and the mechanism of mitochondrial protection, and external toxic brain injury models and treatment animal experiments are also needed [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effect of Gallocatechin Gallate on Glutamate-Induced Oxidative Stress in Hippocampal HT22 Cells

Park

Kang

et al. 2021

Molecules

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Oxidative stress leads to protein degeneration or mitochondrial dysfunction, causing neuronal cell death. Glutamate is a neurotransmitter that nerve cells use to send signals. However, the excess accumulation of glutamate can cause excitotoxicity in the central nervous system. In this study, we deciphered the molecular mechanism of catechin-mediated neuroprotective effect on glutamate-induced oxidative stress in mouse hippocampal neuronal HT22 cells. Cellular antioxidant activity was determined using the 1,1-diphenyl-picryl hydrazyl (DPPH) assay and 2′,7′-dichlorodihydrofluorescein diacetate (DCFDA) staining. Furthermore, the levels of intracellular calcium (Ca2+) as well as nuclear condensation and protein expression related to neuronal damage were assessed. All five catechins (epigallocatechin gallate, gallocatechin gallate (GCG), gallocatechin, epicatechin gallate, and epicatechin) showed strong antioxidant effects. Among them, GCG exhibited the highest neuroprotective effect against glutamate excitotoxicity and was used for further mechanistic studies. The glutamate-induced increase in intracellular Ca2+ was reduced after GCG treatment. Moreover, GCG reduced nuclear condensation and the phosphorylation of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinases (JNK) involved in cell death. The neuroprotective effect of GCG against glutamate-induced oxidative stress in HT22 cells was attributed to the reduction in intracellular free radicals and Ca2+ influx and also the inhibition of phosphorylation of ERK and JNK. Furthermore, the antioxidant effect of GCG was found to be likely due to the inhibition of phosphorylation of ERK and JNK that led to the effective suppression of neurocytotoxicity caused by glutamate in HT22 cells.

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Section: Discussionmentioning

confidence: 99%