Transient Protective Effect of B-Vitamins in Experimental Epilepsy in the Mouse Brain

Abstract

The regulation of programmed cell death in the nervous system of vertebrates is a complex mechanism aimed to remove superfluous or damaged cells. Epileptic seizures can lead to an activation of pathways resulting in neuronal cell death. B-vitamins might have a neuroprotective potential reducing cell death following appropriate stimulation. Here, the role of the B-vitamins B(1) (thiamine), B(6) (pyridoxine), and B(12) (cobalamine) was investigated in a mouse model of experimental epilepsy induced by kainate. B-vitamin pre-treated animals showed a significantly reduced epileptic score during the first 15 min after kainate injection. The molecular response to kainate showed a bi-phased time course with early induction of Bcl-2 expression within 12 h and a second induction after 7 days of kainate exposure. B-vitamin pre-treatment resulted in significant higher Bcl-2 expression in control animals (no kainate) and at 12 h within the early phase. Bcl-2 expression was not affected by B-vitamins within the second phase. BAX expression was not significantly influenced during the whole experiment. Three days after kainate stimulation, the number of TdT-mediated dUTP-biotin nick end labeling-positive cells in the hippocampal region was lower in B-vitamin-treated animals. Therefore, B-vitamin pre-treatment may attenuate the response to epileptic stimulation.

Role of Oxidative Stress in Refractory Epilepsy: Evidence in Patients and Experimental Models

“…Molecules, such as vitamins C and E, glutathione, and coenzyme Q10 (CoQ10), lipoic acid and melatonin, play an important role in the endogenous defensive strategy against oxygen FR [114–129]. Mitochondrial gene therapy (studies targeting the amelioration of mtDNA lesion) [130–132], and substitution of defective mtDNA using gene-carrying vectors to send recombinant mtDNA into cells, are other approaches for mitochondrial gene therapy.…”

The Beneficial Role of Thiamine in Parkinson Disease

“…Therefore, decreased Bcl‐2 protein levels suggest increased levels of apoptosis in patients with PD. However, pretreatment with B vitamins (B 1 , B 6 , and B 12 ) had a protective effect on experimentally induced epilepsy of the mouse brain, which was associated with the induction of Bcl‐2 expression within 12 h of treatment . Moreover, thiamine deprivation was shown to increase cell death and reduce Bcl‐2 expression during hybridoma cell culture .…”

miR‑371b‑5p inhibits endothelial cell apoptosis in monocrotaline‑induced pulmonary arterial hypertension via PTEN/PI3K/Akt signaling pathways

“…Increasing evidence indicates that the PI3K/Akt signaling pathway is involved in vasoconstriction and remodeling ( 10 ), and this signaling pathway is an important target of vasofunctional drugs ( 10 ). A vascular ring model in vitro revealed that a vasoactive intestinal peptide relaxed the mouse pulmonary arterial ring, which may occur through the activation of the pulmonary vascular endothelial cell PI3K/Akt signaling pathway ( 11 ). Additionally, another study reported that estrogen may activate the PI3K/Akt signaling pathway.…”

“…Additionally, another study reported that estrogen may activate the PI3K/Akt signaling pathway. In this manner, PI3K/Akt can regulate the bioactivity of pulmonary vascular system ( 11 ). These studies have indicated that regulating the PI3K/Akt-eNOS signaling pathway is of great importance in the treatment of PAH ( 9 , 11 ).…”

“…In this manner, PI3K/Akt can regulate the bioactivity of pulmonary vascular system ( 11 ). These studies have indicated that regulating the PI3K/Akt-eNOS signaling pathway is of great importance in the treatment of PAH ( 9 , 11 ). In the present study, the function of miR-371b-5p in monocrotaline-induced PAH and the underlying mechanisms were investigated.…”