Effects of Jobelyn® on Isoniazid-Induced Seizures, Biomarkers of Oxidative Stress and Glutamate Decarboxylase Activity in Mice
| Autor: | Adaeze Adebesin, Solomon Umukoro, Abayomi M. Ajayi, Adewale G. Bakre, Stephen Babajide Asehinde, Osarume Omorogbe |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
Glutamate decarboxylase
Status epilepticus Pharmacology medicine.disease_cause lcsh:RC321-571 GABA 03 medical and health sciences Cellular and Molecular Neuroscience chemistry.chemical_compound 0302 clinical medicine Seizures Isoniazid medicine lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry Glutamate decarboxylase activity Glutathione Sorghum bicolor Pyridoxine Malondialdehyde chemistry 030220 oncology & carcinogenesis Neurology (clinical) medicine.symptom 030217 neurology & neurosurgery Oxidative stress Research Paper medicine.drug |
| Zdroj: | Basic and Clinical Neuroscience Basic and Clinical Neuroscience, Vol 9, Iss 6, Pp 389-396 (2018) |
| ISSN: | 2008-126X 2228-7442 |
| Popis: | Introduction Isoniazid-induced seizure, often described as Status Epilepticus (SE), is an emergency condition characterized by repeated convulsive episodes that responds poorly to the currently available anticonvulsant drugs. The current study aimed at ascertaining the effect of Jobelyn® (JB), an African dietary supplement, on seizures, altered oxidative stress, and glutamate decarboxylase activity induced by isoniazid in mice. Methods A total of 6 mice received JB (10-50 mg/kg, PO), pyridoxine (300 mg/kg), diazepam (5 mg/kg), or distilled water (10 mL/kg) 30 minutes prior to the induction of SE with injection of isoniazid (300 mg/kg, IP). Thereafter, the mice were observed for the onset of convulsions for a period of two hours. Moreover, the effect of JB on Glutamate Decarboxylase (GAD) activity and biomarkers of oxidative stress (glutathione and malondialdehyde) was also evaluated in the brain homogenates of another set of isoniazid-treated mice. Results JB (50 mg/kg, PO) prolonged the latency to convulsions, but could not prevent the occurrence of seizure episodes caused by isoniazid. Moreover, JB neither showed any protection against death nor delayed the latency to death caused by isoniazid. However, this dose of JB positively modulated the concentrations of malondialdehyde and glutathione in the brains of mice treated with isoniazid. The activity of GAD, the enzyme responsible for GABA synthesis, increased by JB, which suggested enhanced GABAergic neurotransmission. Conclusion The current study findings suggest that JB prolongs the latency to convulsions, enhances GABAergic neurotransmission, and demonstrates anti-oxidative effect in isoniazid-treated mice. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|