Effect of γ-Aminobutyric Acid on Patients with Refractory Epilepsy

Xinchao Yang¹, Xu Li², Yuanxiu Wang^1, , Chunjiang Ye¹, Yuehui Liu¹, Fang Wang¹, Naxin Sun¹ and Bin Wang³

¹School of Biological Science and Technology, University of Jinan, Jinan 250022, China

²China Resources Shenghai Healthy Technology Co., ltd., Zibo, China

³Shandong Huamei Biotechnology Co. Ltd., Jinan, China

Cite this paper:
Xinchao Yang, Xu Li, Yuanxiu Wang, Chunjiang Ye, Yuehui Liu, Fang Wang, Naxin Sun and Bin Wang. Effect of γ-Aminobutyric Acid on Patients with Refractory Epilepsy. Journal of Food and Nutrition Research. 2024; 12(2):68-74. doi: 10.12691/jfnr-12-2-1

Abstract

This study used mice as experimental materials to study the effects of γ-aminobutyric acid (GABA), rose and tryptophan on epilepsy. In addition, the combination of GABA, rose and tryptophan was studied to alleviate epilepsy. The optimal dosage of GABA, tryptophan and rose were determined to be 100 mg/kg, 160 mg/kg and 1.6 g/kg, respectively, according to the behavior of mice and oxidative stress indexes in serum. Screening the combination of GABA-compatible functional substances that can improve epilepsy, the optimal concentrations of GABA+ rose, GABA+ tryptophan, GABA+ rose + tryptophan were determined to be 10 mg/kg+1.4 g/kg, 10 mg/kg+170 mg/kg, 10 mg/kg+1.4 g/kg+170 mg/kg. Three kinds of whole nutrition food with the ability to relieve epilepsy in mice were obtained: GABA+ tryptophan (formula food 1), GABA+ rose (formula food 2), and tryptophan (formula food 3). Results showed that the three products had no significant effect on the body weight of mice, and the incubation period of epileptic seizure of mice was prolonged by 1 min. Meanwhile, the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) in serum increased, while the content of malondialdehyde (MDA) decreased. Combined with the new nutrition knowledge and advanced food processing technology, three kinds of whole nutrition medical food were prepared. This food has a good effect of relieving epilepsy, but also can meet the normal nutrient needs.

Keywords:
GABA epilepsy medical food

This work is licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

References:

[1]	Hoyt CT, Do mingo-Fernández D, Balzer N, et al. A systematic approach for identifying shared mechanisms in epilepsy and its comorbidities [J]. Database(Oxford), 2018, 18: 1-9
[2]	Han H A, Cortez M A, Snead O C. GABA-B Receptor and Absence Epilepsy [J]. National Center for Biotechnology Information (US), 2012, 80: 242-256
[3]	Carmona-Aparicio L, Pérez-Cruz C, Zavala-Tecuapetla C, et al. Overview of nrf2 as therapeutic target in epilepsy [J]. International Journal of Molecular Sciences, 2015, 16(8): 18348-18367.
[4]	Franco D, Pinelo M, Sineiro J. Processing of Rosarubiginosa:Extraction of oil and antioxidant substances [J]. Bioresour Technol, 2007, 98(18): 3506-3512.
[5]	Xu W, Orr-Urtreger A, Nigro F, et al. Multiorgan autonomic dysfunction in mice lacking the beta2 and the beta4 subunits of neuronal nicotinic acetylcholine receptors [J]. J Neurosci, 1999, 19(21): 9298-9305.
[6]	Zhao H, Lin Y, Chen S, et al. 5-HT3 receptors: a potential therapeutic target for epilepsy [J]. Curr Neuropharmacol, 2018, 16(1): 29-36.
[7]	Wheless J W. History of the ketogenic diet [J]. Epilepsia, 2008, 49 (Suppl 8): 3-5.
[8]	Oga B, Uu C, Na D. Efficacy and tolerability of olive oil-based ketogenic diet in children with drug-resistant epilepsy: A single center experience from Turkey [J]. European Journal of Paediatric Neurology, 2019, 23(1): 143-151.
[9]	Kossoff E H, Nabbout R. Use of dietary therapy for status epilepticus [J]. Journal of Child Neurology, 2013, 28(8): 1049-1051.
[10]	Misiewicz Runyon A, So T Y. The use of ketogenic diet in pediatric with epilepsy [J]. ISRN Pediatrics, 2012 (2012): 1-10.
[11]	Nei M, Ngo L, Sirven JI, et al. Ketogenic diet in adolescents and adults with epilepsy[J]. Seizure, 2014, 23(6): 439-442.
[12]	Allen B G, Bhatia S K, Anderson C M, et al. Ketogenic diets as an adjuvant cancer therapy: History and potential mechanism [J]. Redox Biol, 2014, (2): 963-970.
[13]	Yancy W S, Westman E C, McDuffie J R, et al. A randomized trial of a low-carbohydrate diet vs orlistat plus a low-fat diet for weight loss [J]. Arch Int Med, 2010, 170(2): 136–145.
[14]	Kossoff E H, Turner Z, Bluml R M, et al. A randomized, crossover comparison of daily carbohydrate limits using the modified Atkins diet [J]. Epilepsy & Behavior, 2007, 10(3): 432-436.
[15]	Racine RJ. Modification of seizure activity by electrical stimulation I After-discharge threshold [J]. Electroencephalogr Clin Neurophysiol, 1972, 32(3): 269-279．
[16]	Freitas R M D, Nascimento K G D, Ferreira P M P, et al. Neurochemical changes on oxidative stress in rat hippocampus duringacute phase of pilocarpine-induced seizures [J]. Pharmacology Biochemistry and Behavior, 2010, 94: 341-345.