The modulator action of thiamine against pentylenetetrazole-induced seizures, apoptosis, nitric oxide, and oxidative stress in rats and SH-SY5Y neuronal cell line

Taşkıran, Ahmet Şevki; Ergül, Mustafa

doi:10.1016/j.cbi.2021.109447

Cited by 29 publications

(11 citation statements)

References 48 publications

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“…25) Previous studies have reported that thiamine protects tissues from oxidative damage by increasing antioxidant enzymes, CAT and SOD, and reducing lipid peroxidation. 26,27) Consistent with these studies, in this study thiamine pretreatment increased antioxidant enzymes, SOD and CAT, levels and also decreased MDA levels, which is a marker of oxidative damage after glutamate exposed cytotoxicity in the C6 cells.…”

Section: Discussionsupporting

confidence: 88%

Thiamine Protects Glioblastoma Cells against Glutamate Toxicity by Suppressing Oxidative/Endoplasmic Reticulum Stress

Ergül

Taşkıran

2021

Chem. Pharm. Bull.

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Thiamine (vitamin B1), which is synthesized only in bacteria, fungi and plants and which humans should take with diet, participates in basic biochemical and physiological processes in a versatile way and its deficiency is associated with neurological problems accompanied by cognitive dysfunctions. The rat glioblastoma (C6) model was used, which was exposed to a limited environment and toxicity with glutamate. The cells were stressed by exposure to glutamate in the presence and absence of thiamine. The difference in cell proliferation was evaluated in the XTT assay. Oxidative stress (OS) markers malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) levels, as well as endoplasmic reticulum (ER) stress markers 78-kDa glucose-regulated protein (GRP78), activating transcription factor-4 (ATF-4), and C/EBP homologous protein (CHOP) levels, were measured with commercial kits. Apoptosis determined by flow cytometry was confirmed by 4′,6-diamidino-2-phenylindole (DAPI) staining. At all concentrations, thiamine protects the cells and increased the viability against glutamate-induced toxicity. Thiamine also significantly decreased the levels of MDA, while increasing SOD and CAT levels. Moreover, thiamine reduced ER stress proteins' levels. Moreover, it lessened the apoptotic cell amount and enhanced the live-cell percentage in the flow cytometry and DAPI staining. As a result, thiamine may be beneficial nutritional support for individuals with a predisposition to neurodegenerative disorders due to its protective effect on glutamate cytotoxicity in glioblastoma cells by suppressing OS and ER stress.

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Section: Discussionsupporting

confidence: 88%

Thiamine Protects Glioblastoma Cells against Glutamate Toxicity by Suppressing Oxidative/Endoplasmic Reticulum Stress

Ergül

Taşkıran

2021

Chem. Pharm. Bull.

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“…MDA, as the by-product of the peroxidation of polyunsaturated fatty acids, is toxic to neurons and plays a crucial role in the induction of neuroinflammation. An increase in its brain levels leads to the progression of epilepsy through destabilization of the lipid membrane ( 79 ). There is a positive correlation between plasma MDA level and seizure severity in patients with epilepsy ( 80 , 81 ).…”

Section: Discussionmentioning

confidence: 99%

Influence of methadone on the anticonvulsant efficacy of valproate sodium gabapentin against maximal electroshock seizure in mice by regulation of brain MDA TNF-α

Jafari

Hassanpour-Ezatti

2022

Front. Neurol.

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Methadone is the most frequently used opioid therapy worldwide, with controversial effects on oxidative stress homeostasis. This study investigated the effects of intraperitoneal (i.p.) co-administration of methadone (0.1, 0.3, 1, and 3 mg/kg) and valproate sodium (300 mg/kg) or gabapentin (50 mg/kg) in the mice maximal electroshock (MES)-induced seizure model. The adverse effect of drugs was assessed using the chimney test. The levels of tumor necrosis factor-alpha (TNF-α) and malondialdehyde (MDA) contents were measured in mice brains after a single seizure. Administration of methadone alone resulted in a significant reduction in the duration of hind limb extension (HLE) than that in the control group. Methadone pretreatment at doses of 0.1 and 0.3 mg/kg i.p. decreased, and at doses of 1 and 3 mg/kg i.p. had an increasing effect on anticonvulsant efficacy of gabapentin. Pretreatment with all doses of methadone significantly decreased the valproate anticonvulsive efficacy. At doses of 1 and 3 mg/kg i.p. methadone per se increased brain MDA levels after MES-induced seizure. Administration of methadone (0.3 mg/kg i.p.) enhanced and at 3 mg/kg decreased gabapentin effect on brain MDA level, but their co-treatment did not lead to further increase in MDA. Methadone at 0.3–3 mg/kg enhanced the effect of sodium valproate on MDA levels in the brain, but at all doses significantly potentiated its effect on brain TNF-α levels. The drugs did not produce any side effects on motor coordination in experimental animals. In conclusion, methadone showed different effects on anticonvulsant actions of gabapentin and valproate through regulation of brain levels of MDA and TNF-α.

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“…Our results also showed that thiamine pretreatment alleviated learning de cits caused by PTZ-kindling. Thiamine is a neuroin ammation modulator known for removing reactive oxidative species (Liu et al 2017;Taskiran and Ergul 2021). Also, previous studies reported that benfotiamine can exert antiin ammatory effects (Sánchez-Ramírez et al 2006;Shoeb and Ramana 2012).…”

Section: Discussionmentioning

confidence: 99%

Thiamine Alleviates Cognitive Impairment and Epileptogenesis by Relieving Brain Inflammation in PTZ-induced Kindling Rat Model

Karabulut

Filiz

Akkaya

2021

Preprint

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Epileptogenesis, the process by which the brain becomes epileptic, is related to neuroinflammation, hyperexcitability, and as a result cognitive deficits. Evidence suggests that therapeutic strategies targeting pathologic brain inflammation have emerged as a promising approach that prevents or disease-modifying therapy for epileptogenesis. Therefore, the PTZ kindling model of epilepsy was utilized to assess the neuroprotective role of thiamine in epileptogenesis. Male rats were exposed to PTZ-induced kindling and pretreated with low thiamine (25 mg/kg) or high thiamine (50 mg/kg). Cyclooxygenase (COX-1 and COX-2), interleukin 1-beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and nuclear factor-κB (NF-κB) concentrations in the brain were analyzed using biochemical assays. Cognitive function was evaluated using the passive avoidance test. Thiamine ameliorated epileptogenesis and enhanced the rats' performance in the passive avoidance test. Also, thiamine significantly decreased the level of neuroinflammatory mediators in the brain induced by PTZ. These results provide evidence that thiamine alleviates PTZ-induced neuroinflammation and cognitive impairments.

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The modulator action of thiamine against pentylenetetrazole-induced seizures, apoptosis, nitric oxide, and oxidative stress in rats and SH-SY5Y neuronal cell line

Cited by 29 publications

References 48 publications

Thiamine Protects Glioblastoma Cells against Glutamate Toxicity by Suppressing Oxidative/Endoplasmic Reticulum Stress

Thiamine Protects Glioblastoma Cells against Glutamate Toxicity by Suppressing Oxidative/Endoplasmic Reticulum Stress

Influence of methadone on the anticonvulsant efficacy of valproate sodium gabapentin against maximal electroshock seizure in mice by regulation of brain MDA TNF-α

Thiamine Alleviates Cognitive Impairment and Epileptogenesis by Relieving Brain Inflammation in PTZ-induced Kindling Rat Model

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