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Acteoside Isolated from Colebrookea oppositifolia Smith Attenuates Epilepsy in Mice Via Modulation of Gamma-Aminobutyric Acid Pathways.

Authors
  • Viswanatha, Gollapalle Lakshminarayanash...1
  • Shylaja, Hanumanthappa2
  • Kishore, Darisi Venkata3
  • Venkataranganna, Marikunte V4
  • Prasad, Nunna Bheema Lingeswara5
  • 1 , Bangalore, India. [email protected] , (India)
  • 2 , Bangalore, India. , (India)
  • 3 Shadan College of Pharmacy. (SCOP) Peerancheru, Hyderabad, 500086, India. , (India)
  • 4 Connexios Life Sciences Pvt Ltd, Basavanagudi, Bangalore, 560 004, India. , (India)
  • 5 Oil Technological and Pharmaceutical Research Institute (OTPRI), JNT University Anantapur, Ananthapuramu, 515 002, India. , (India)
Type
Published Article
Journal
Neurotoxicity Research
Publisher
Springer-Verlag
Publication Date
Dec 01, 2020
Volume
38
Issue
4
Pages
1010–1023
Identifiers
DOI: 10.1007/s12640-020-00267-0
PMID: 32803629
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

The present study was aimed to evaluate the anticonvulsant activity of acteoside and explore its mechanism of action. Initially, the acteoside was evaluated in maximal electroshock (MES) and pentylenetetrazole (PTZ)-induced convulsions, and later it was evaluated against N-methyl-D-aspartic acid (NMDA)-induced mortality in Swiss albino mice. Based on the response in these models, further evaluations were performed to explore the mechanism of action. In the results, the acteoside (10, 25, and 50 mg/kg) has shown significant anticonvulsant activity in the PTZ model (p < 0.01 for all doses); however, there was no protection observed in MES and NMDA models. Therefore, further mechanism-based studies were performed on the PTZ model, and the outcomes have revealed that there was a significant reduction in GABA (p < 0.01 for both regions) and elevation of glutamate (p < 0.01 for both regions) in the cortex and hippocampus regions of PTZ-treated animals. Further, the antioxidant levels (SOD, catalase, GPx, GR, GSH, LPO) were altered significantly (p < 0.01 for all parameters), with reduced GABAA mRNA levels (p < 0.01) in the PTZ control compared with the normal control. Interestingly, co-administration of acteoside (25 mg/kg) (p < 0.01 for all parameters) has restored all the PTZ-induced alterations compared to PTZ-control. Moreover, the anti-PTZ action of acteoside was completely blocked in the presence of flumazenil, and thus confirmed the GABAergic mechanism behind the anticonvulsant activity of acteoside. Besides, actophotometer and rotarod tests have confirmed that the acteoside is free from central side effects like motor incoordination and locomotor deficits.

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