Protective effect of gamma‐aminobutyric acid against oxidative stress by inducing phase II enzymes in C2C12 myoblast cells

Author(s):  
Hyeonjeong Choe ◽  
Hana Lee ◽  
Junsoo Lee ◽  
Younghwa Kim

2021 ◽  
Vol 22 (3) ◽  
pp. 1285
Author(s):  
Seong Soon Kim ◽  
Hyemin Kan ◽  
Kyu-Seok Hwang ◽  
Jung Yoon Yang ◽  
Yuji Son ◽  
...  

Epilepsy is one of the most common neurological disorders, and it is characterized by spontaneous seizures. In a previous study, we identified 4-(2-chloro-4-fluorobenzyl)-3-(2-thienyl)-1,2,4-oxadiazol-5(4H)-one (GM-90432) as a novel anti-epileptic agent in chemically- or genetically-induced epileptic zebrafish and mouse models. In this study, we investigated the anti-epileptic effects of GM-90432 through neurochemical profiling-based approach to understand the neuroprotective mechanism in a pentylenetetrazole (PTZ)-induced epileptic seizure zebrafish model. GM-90432 effectively improved PTZ-induced epileptic behaviors via upregulation of 5-hydroxytryptamine, 17-β-estradiol, dihydrotestosterone, progesterone, 5α -dihydroprogesterone, and allopregnanolone levels, and downregulation of normetanephrine, gamma-aminobutyric acid, and cortisol levels in brain tissue. GM-90432 also had a protective effect against PTZ-induced oxidative stress and zebrafish death, suggesting that it exhibits biphasic neuroprotective effects via scavenging of reactive oxygen species and anti-epileptic activities in a zebrafish model. In conclusion, our results suggest that neurochemical profiling study could be used to better understand of anti-epileptic mechanism of GM-90432, potentially leading to new drug discovery and development of anti-seizure agents.



2013 ◽  
Vol 22 (2) ◽  
pp. 485-491 ◽  
Author(s):  
Younghwa Kim ◽  
Youngmin Choi ◽  
Hyeonmi Ham ◽  
Heon-Sang Jeong ◽  
Junsoo Lee


2013 ◽  
Vol 26 (3) ◽  
pp. 485-491
Author(s):  
Bo-Ra Yoon ◽  
Young-Hyun Kim ◽  
Jong-Seok Lee ◽  
Hee-Do Hong ◽  
Young-Kyoung Rhee ◽  
...  


2020 ◽  
Vol 10 ◽  
Author(s):  
S. Navaneetha Krishnan ◽  
T. Divya ◽  
R. Jayaraman ◽  
P. Latha ◽  
Narahari N Palei ◽  
...  

Background: Sunset Yellow is a commonly used synthetic food additive in various food beverages. Over usage of this colorant induce the anxiogenic behaviour in mice through oxidative stress. Vernonia cinerea reverses anxiogenic behaviour by counteracting oxidative stress. Objective: The study was designed to screen the protective effect of Vernonia cinerea extract against sunset yellow induced anxiogenic behaviour in mice through counteracting oxidative damage. Methods: The anxiogenic effect was induced by the administration of sunset yellow (20 mg/kg, p.o) for 30 days. Ethanol extract of Vernonia cinerea (EEVC) aerial parts (400 mg/kg, p.o) administered, after 1 hour of sunset yellow treatment. Diazepam (1 mg/kg, p.o) was used as a reference drug for comparisons. Results: FT-IR studies of the extract were done by comparing with standards to determine the presence of phenols and flavonoids. Vernonia cinerea significantly improved the altered anxiogenic behaviour of sunset yellow treated animals. Significant increase in the brain antioxidant enzymes catalase (CAT), superoxide dismutase (SOD) and neurotransmitter Gamma-aminobutyric acid (GABA) level and decrease the lipid peroxidation and glutamate neurotransmitter was observed in Vernonia cinerea treated group and also this extract reversed the hippocampus CA3 region abnormalities such as perivascular oedema, haemorrhage and severe vocalisation in sunset yellow group. Conclusion: The Vernonia cinerea possesses significant antioxidant, antiradical and GABA enhancing effects against sunset yellow induced anxiogenic animals.



2019 ◽  
Vol 39 (2) ◽  
pp. 159-172 ◽  
Author(s):  
MA Al Kahtani

Because cadmium (Cd) is not naturally degradable by ecosystems, it interferes with many types of food chains. Cd accumulates in the kidney, liver and in the nervous tissues, especially the brain. The neurotoxicity of Cd is very high, as it alters the integrity, and increases the permeability, of the blood–brain barrier. Cd penetrates and accumulates in neurons in the brains of rats. This study reveals that Cd decreases antioxidant enzymes and increases oxidative stress in the brain. In addition, Cd increases lipid peroxidation of brain tissues. Cd increases the expression of the Cu/Zn superoxide dismutase gene. It also affects cholinergic, glutamatergic, gamma-Aminobutyric acid (GABAergic), dopamine, serotonin and acetylcholine neurotransmitters in brain tissue. Consequently, Cd increases the formation of amyloid β, a neurotoxic index, and induces apoptosis by changing the quality and the quantity of Bcl-2, Bax and p53 proteins. In conclusion, both selenium and nanoselenium show potential antioxidant activity and promote recovery from the neurotoxic action of Cd.







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