Acta Scientific Neurology (ASNE) (ISSN: 2582-1121)

Research Article Volume 4 Issue 5

Pharmacotherapeutic Effects of Hippophae rhamnoides in Rat Model of Post-traumatic Epilepsy in View of Oxidative Stress, Na+,K+ATPase Activity and Sodium Ion Channel Expression

Stanzin Ladol1,2* and Deepak Sharma2

1Department of Zoology, Central University of Jammu, Bagla (Rahya Suchani) Distt. Samba, Jammu and Kashmir, India
2Neurobiology Laboratory, School of Life Sciences, Jawaharlal Nehru University, New Delhi, India

*Corresponding Author: Stanzin Ladol, Department of Zoology, Central University of Jammu, Bagla (Rahya Suchani) Distt. Samba, Jammu and Kashmir, India.

Received: March 11, 2021; Published: May 07, 2021

Abstract

Background: Post-traumatic epilepsy (PTE) is a brain disorder characterized by an occurrence of spontaneous and recurrent seizures post brain insults. Initiation and progression of epilepsy is a complex process involving numerous cellular, molecular, and signalling mechanisms. Therefore, understanding the mechanism involved and finding safer treatments is of paramount importance.

Objectives and Methods: In this study, the antiepileptic effect of Hippophae rhamnoides (sea buckthorn/sbt) in post-traumatic epilepsy model was assessed. Post-traumatic epilepsy was induced by intracortical iron (5μl of 100mM FeCl3) injection. Hippophae rhamnoides berry extract was administered orally at a dose of 1ml/kg b.wt. for 1 month. Then, the effect of sbt on the oxidative stress, Na+,K+ATPase activity and sodium ion channel expression was evaluated.

Results and Discussions: In cortex and hippocampus of epileptic rats, the results demonstrate altered electrophysiology, elevated oxidative stress, and reduced antioxidant defense. Additionally, reduced Na+,K+ATPase activity and elevated sodium channel Nav1.1 and Nav1.6 expression were also observed. Sbt administration has attenuated epileptiform activity, counteracted oxidative stress, elevated Na+,K+ATPase activity, and decreased sodium channel expression in the cortex and hippocampus of epileptic rats. In summary, our results demonstrate the antiepileptic effect of sbt that have possibly exerted by its antioxidative and ion channel regulatory properties in post-traumatic epilepsy model.

Keywords: Post-traumatic Epilepsy; Iron-induced Epilepsy; Hippophae rhamnoides; Sea Buckthorn; Seizure

References

  1. Lowenstein DH. “Epilepsy after head injury: an overview”. Epilepsia 50 (2009): 4-9.
  2. Webster KM., et al. “Progesterone treatment reduces neuroinflammation, oxidative stress and brain damage and improves long-term outcomes in a rat model of repeated mild traumatic brain injury”. Journal of Neuroinflammation 12 (2015): 238.
  3. Cruz-Haces M., et al. “Pathological correlations between traumatic brain injury and chronic neurodegenerative diseases”. Translational Neurodegeneration 6 (2017): 20.
  4. Campbell JN., et al. “Traumatic brain injury causes a tacrolimus-sensitive increase in non-convulsive seizures in a rat model of post-traumatic epilepsy”. International Journal of Brain Disorders and Treatment 1 (2014): 1-11.
  5. Willmore LJ., et al. “Recurrent seizures induced by cortical iron injection: a model of posttraumatic epilepsy”. Annals of Neurology 4 (1978): 329-336.
  6. Mittler R. “Oxidative stress, antioxidants and stress tolerance”. Trends in Plant Science 7 (2002): 405-410.
  7. Shao HB., et al. “Primary antioxidant free radical scavenging and redox signaling pathways in higher plant cells”. International Journal of Biological Sciences 4 (2008) 8.
  8. Mishra M., et al. “Antiepileptic action of exogenous dehydroepiandrosterone in iron-induced epilepsy in rat brain”. Epilepsy Behavior 19 (2010): 264-271.
  9. Negre-Salvayre A., et al. “Pathological aspects of lipid peroxidation”. Free Radical Research 44 (2010): 1125-1171.
  10. Das J., et al. “Antiepileptic effect of fisetin in iron-induced experimental model of traumatic epilepsy in rats in the light of electrophysiological, biochemical, and behavioural observations”. Nutrition and Neuroscience 20 (2017): 255-264.
  11. Kumar V., et al. “Curcumin’s antiepileptic effect, and alterations in Nav1.1 and Nav1.6 expression in iron-induced epilepsy”. Epilepsy Research 150 (2019): 7-16.
  12. Silva LFA., et al. “The involvement of Na+, K+-ATPase activity and free radical generation in the susceptibility to pentylenetetrazol-induced seizures after experimental traumatic brain injury”. Journal of the Neurological Sciences 308 (2011): 35-40.
  13. Klein JP., et al. “Dysregulation of sodium channel expression in cortical neurons in a rodent model of absence epilepsy”. Brain Research 1000 (2004): 102-109.
  14. Duflocq A., et al. “Nav1. 1 is predominantly expressed in nodes of Ranvier and axon initial segments”. Molecular and Cellular Neuroscience 39 (2008): 180-192.
  15. Caldwell JH., et al. “Sodium channel Nav1. 6 is localized at nodes of Ranvier, dendrites, and synapses”. Proceedings of the National Academy of Sciences of the United States of America 97 (2000): 5616-5620.
  16. Blumenfeld H., et al. “Role of hippocampal sodium channel Nav1.6 in kindling epileptogenesis”. Epilepsia 50 (2009): 44-55.
  17. Xu X., et al. “Abnormal changes in voltage-gated sodium channel NaV1. 1, NaV1. 2, NaV1. 3, NaV1. 6 and in calmodulin/calmodulin-dependent protein kinase II, within the brains of spontaneously epileptic rats and tremor rats”. Brain Research Bulletin 96 (2013): 1-9.
  18. Volk HA and Löscher W. “Multidrug resistance in epilepsy: rats with drug-resistant seizures exhibit enhanced brain expression of P-glycoprotein compared with rats with drug-responsive seizures”. Brain 128 (2005): 1358-1368.
  19. Aycicek A and Iscan A. “The effects of carbamazepine, valproic acid and phenobarbital on the oxidative and antioxidative balance in epileptic children”. European Neurology 57 (2007): 65-69.
  20. Fernandez MT., et al. “Iron and copper chelation by flavonoids: an electrospray mass spectrometry study”. Journal of Inorganic Biochemistry 92 (2002): 105-111.
  21. Suryakumar G and Gupta A. “Medicinal and therapeutic potential of Sea buckthorn (Hippophae rhamnoides L.)”. Journal of Ethnopharmacology 138 (2011): 268-278.
  22. Yang B and Kallio HP. “Fatty acid composition of lipids in sea buckthorn (Hippophae rhamnoides L.) berries of different origins”. Journal of Agricultural and Food Chemistry 49 (2001): 1939-1947.
  23. Seifried HE., et al. “A review of the interaction among dietary antioxidants and reactive oxygen species”. Journal of Nutritional Biochemistry 18 (2007): 567-579.
  24. Luís Â., et al. “Interactions between the major bioactive polyphenols of berries: effects on antioxidant properties”. European Food Research and Technology 244 (2018): 175-185.
  25. Batool F., et al. “Oral supplementation of Sea buckthorn (Hippophae rhamnoides L. Spp. Turkestanica) fruit extract modifies haloperidol induced behavioral deficits and increases brain serotonin metabolism”. Journal of Food and Drug Analysis 17 (2009): 257-263.
  26. Paxinos G and Watson C. “The rat brain in stereotaxic coordinates: hard cover edition”. Elsevier (2010).
  27. Lowry OH., et al. “Protein measurement with the Folin phenol reagent”. Journal of Biological Chemistry 193 (1951): 265-275.
  28. Ohkawa H., et al. “Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction”. Analytical Biochemistry 95 (1979): 351-358.
  29. Marklund S and Marklund G. “Involvement of the superoxide anion radical in the autoxidation of pyrogallol and a convenient assay for superoxide dismutase”. European Journal of Biochemistry 47 (1974): 469-474.
  30. Claiborne AL. “Catalase activity”. Greenwald, R.A. (Ed.), CRC handbook of methods for oxygen radical research. CRC Press, Boca Raton, FL (1986).
  31. Beltowski J., et al. “Regulation of renal Na, K-ATPase and ouabain-sensitive H, K-ATPase by the cyclic AMP-protein kinase A signal transduction pathway”. Acta Biochimica Polonica 50 (2003): 103-114.
  32. McNamara JO., et al. “Molecular signaling mechanisms underlying epileptogenesis”. Science Signaling 356 (2006): re12.
  33. Gorter JA., et al. “Status epilepticus, blood-brain barrier disruption, inflammation, and epileptogenesis. Epilepsy Behavior 49 (2015): 13-16.
  34. Sharma V., et al. “Iron-induced experimental cortical seizures: electroencephalographic mapping of seizure spread in the subcortical brain areas”. Seizure 16 (2007): 680-690.
  35. Sethi P., et al. “Aluminium-induced electrophysiological, biochemical and cognitive modifications in the hippocampus of aging rats”. Neurotoxicology 29 (2008): 1069-1079.
  36. Pauletti A., et al. “Targeting oxidative stress improves disease outcomes in a rat model of acquired epilepsy”. Brain Journal of Neurology 142 (2019): e39.
  37. Silva LFA., et al. “Treadmill exercise protects against pentylenetetrazol-induced seizures and oxidative stress after traumatic brain injury”. Journal of Neurotrauma 30 (2013): 1278-1287.
  38. Halliwell B. “Reactive oxygen species and the central nervous system”. Journal of Neurochemistry 59 (1992): 1609-1623.
  39. Prakash C., et al. “Dehydroepiandrosterone alleviates oxidative stress and apoptosis in iron-induced epilepsy via activation of Nrf2/ARE signal pathway”. Brain Research Bulletin 153 (2019): 181-190.
  40. Albarracin SL., et al. “Effects of natural antioxidants in neurodegenerative disease”. Nutrition and Neuroscience 15 (2012): 1-9.
  41. Lees GJ. “Inhibition of sodium-potassium-ATPase: a potentially ubiquitous mechanism contributing to central nervous system neuropathology”. Brain Research Review 16 (1991): 283-300.
  42. Tsakiris S., et al. “Protective effect of L-cysteine and glutathione on the modulated suckling rat brain Na+, K+-ATPase and Mg2+-ATPase activities induced by the in vitro galactosaemia”. Pharmaceutical Research 49 (2004): 475-479.
  43. Bavaresco CS., et al. “Effect of hypoxanthine on Na+, K+-ATPase activity and some parameters of oxidative stress in rat striatum”. Brain Research 1041 (2005): 198-204.
  44. Kinjo ÉR., et al. “The Na+/K+ ATPase activity is increased in the hippocampus after multiple status epilepticus induced by pilocarpine in developing rats”. Brain Research 1138 (2007): 203-207.
  45. Rezin GT., et al. “Evaluation of Na+, K+-ATPase activity in the brain of young rats after acute administration of fenproporex”. Brazilian Journal of Psychiatry 36 (2014): 138-142.
  46. Yamakawa K. “Na channel gene mutations in epilepsy—the functional consequences”. Epilepsy Research 70 (2006): 218-222.
  47. Catterall WA., et al. “NaV1.1 channel and epilepsy”. Journal of Physics 588 (2010): 1849-1859.
  48. Zhu H., et al. “Remarkable alterations of Nav1.6 in reactive astrogliosis during epileptogenesis”. Scientific Report 6 (2016): 38108.

Citation

Citation: Stanzin Ladol and Deepak Sharma. “Pharmacotherapeutic Effects of Hippophae rhamnoides in Rat Model of Post-traumatic Epilepsy in View of Oxidative Stress, Na+,K+ATPase Activity and Sodium Ion Channel Expression”. Acta Scientific Neurology 4.6 (2021): 02-11.

Copyright

Copyright: © 2021 Stanzin Ladol and Deepak Sharma. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.




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