Neuroprotective Effects of Isolated Fraction from Sapindus laurifolia Extract in Hippocampal Neuronal HT22 Cells

Jump To References Section

Authors

  • Nagaraju Bandaru
     Department of Pharmaceutical Sciences, Chebrolu Hanumaiah Institute of Pharmaceutical Sciences, Chowdavaram – 522019, Guntur, Andhra Pradesh ,IN
  • A. Ramu
     Department of Pharmaceutical Sciences, Chebrolu Hanumaiah Institute of Pharmaceutical Sciences, Chowdavaram – 522019, Guntur, Andhra Pradesh ,IN
  • S. Vidhyadhara
     Department of Pharmaceutical Sciences, Chebrolu Hanumaiah Institute of Pharmaceutical Sciences, Chowdavaram – 522019, Guntur, Andhra Pradesh ,IN

DOI:

https://doi.org/10.18311/ti/2020/v27i1&2/25580

Keywords:

Antioxidant, Glutamate, Hippocampal Cells, Neuroprotective, Oxidative Stress

Abstract

Glutamate is a major endogenous excitatory neurotransmitter in the brain and contributes to the development of neurodegenerative diseases by excessive activation. The purpose of the present study was to determine the neuroprotective effect of Sapindus laurifolia (MESL) Fraction A against glutamate-induced oxidative stress and to assess the underlying mechanism. MESL Fraction A was subjected to a neuroprotective effect assay in HT22 mouse hippocampal cells. The mechanism underlying the neuroprotective effect of MESL Fraction A was evaluated by assaying Reactive Oxygen Species (ROS) levels, intracellular Ca2+ levels, mitochondrial membrane potential and glutathione level and antioxidant enzyme activity in HT22 cells. MESL Fraction A significantly decreased glutamate-induced death of HT22 cells (88.23 ± 1.65% relative neuroprotection). MESL Fraction A reduced the intracellular ROS and Ca2+ levels and increased the glutathione level and glutathione reductase and glutathione peroxide activities. Moreover, MESL Fraction A attenuated the mitochondrial membrane potential in HT22 cells. These results suggested that MESL Fraction A exerts a neuroprotective effect against oxidative stress HT22 cells, which was mediated by its antioxidant activity.

Downloads

Download data is not yet available.

Downloads

Published

2020-10-01

How to Cite

Bandaru, N., Ramu, A., & Vidhyadhara, S. (2020). Neuroprotective Effects of Isolated Fraction from <I>Sapindus laurifolia</I> Extract in Hippocampal Neuronal HT22 Cells. Toxicology International, 27(1&amp;2), 79–85. https://doi.org/10.18311/ti/2020/v27i1&2/25580

Issue

Volume 27, Issue 1&2, January-June 2020

Section

Research Articles
Crossref
Scopus
Google Scholar
Europe PMC
Received 2020-07-01
Accepted 2020-08-24
Published 2020-10-01

 

References

Hynd MR, Scott HL, Dodd PR. Glutamate-mediated excitotoxicity and neurodegeneration in Alzheimer's disease. Neurochem Int. 2004 Oct; 45(5):583–95. PMid: 15234100. https://doi.org/10.1016/j.neuint.2004.03.007

Choi DW. Glutamate neurotoxicity in cortical cell cultures is calcium dependent. Neurosci. Lett. 1985; 58(3):293–7. https://doi.org/10.1016/0304-3940(85)90069-2

Tan S, Wood M, Maher P. Oxidative stress induces a form of programmed cell death with characteristics of both apoptosis and necrosis in neuronal cells. J Neurochem. 1998 Jul; 71(1):95–105. PMid: 9648855. https://doi. org/10.1046/j.1471-4159.1998.71010095.x

Murphy TH, Miyamoto M, Sastre A, Schnaar RL, Coyle JT. Glutamate toxicity in neuronal cell line involves inhibition of cystine transport leading to oxidative stress. Neuron. 1989; 2(6):1547–58. https://doi.org/10.1016/0896- 6273(89)90043-3

Swerdlow RH. Pathogenesis of Alzheimer's disease. Clin Interv Aging, 2007; 2(3):347–59.

Liu J, Li L, Suo WZ. HT22 hippocampal neuronal cell line possesses functional cholinergic properties. Life Sci. 2009 Feb; 84(9-10):267–71. PMid: 19135458. https://doi. org/10.1016/j.lfs.2008.12.008

Sakthivel KM, Guruvayoorappan C. Biophytum sensitivum, ancient medicine, modern targets. J Adv Pharm Technol Res. 2012; (3): 83–91. PMid: 22837955 PMCid: PMC3401679. https://doi.org/10.4103/2231-4040.97279

Trease G, Evans SM. Pharmacognosy. 15th ed. London: Bailer Tindal; 2002. p. 23–67.

Yun BR, Yang HJ, Weon JB, Lee J, Eom MR, Ma CJ. Neuroprotective properties of compounds extracted from Dianthus superbus L. against glutamate-induced cell death in HT22 cells. Pharmacogn Mag. 2016 Apr-Jun; 12(46):109–13. PMid: 27076746 PMCid: PMC4809164. https://doi.org/10.4103/0973-1296.177905

Markesbery WR. Oxidative stress hypothesis in Alzheimer's disease. Free Radic Biol Med. 1997; 23(1):134–47. https:// doi.org/10.1016/S0891-5849(96)00629-6

Ankarcrona M, Dypbukt JM, Bonfoco E, Zhivotovsky B, Orrenius S, Lipton SA, Nicotera P, et al. Glutamateinduced neuronal death: A succession of necrosis or apoptosis depending on mitochondrial function. Neuron.1995; 15(4):961–73. https://doi.org/10.1016/0896- 6273(95)90186-8

Duchen M. Mitochondria and calcium: From cell signaling to cell death. J Physiol. 2000; 529(11):57–68. PMid: 11080251 PMCid: PMC2270168. https://doi.org/10.1111/ j.1469-7793.2000.00057.x

Reynolds IJ, Hastings TG. Glutamate induces the production of reactive oxygen species in cultured forebrain neurons following NMDA receptor activation. J Neurosci. 1995; 15:3318–27. PMid: 7751912 PMCid: PMC6578215. https://doi.org/10.1523/JNEUROSCI.15-05-03318.1995

Randall RD, Tayer SA. Glutamate-induced calcium transient triggers delayed calcium overload and neurotoxicity in rat hippocampal neurons. J Neurosci. 1992; 12(5):1882–95. PMid: 1349638 PMCid: PMC6575874. https://doi. org/10.1523/JNEUROSCI.12-05-01882.1992

Koga M, Serritella AV, Messmer MM, Hayashi-Takagi A, Hester LD, Snyder SH, Sawa A, Sedlak TW. Glutathione is a physiologic reservoir of neuronal glutamate. Biochem Biophys Res Commun. 2011; 409(4):596–602. PMid: 21539809 PMCid: PMC3923312. https://doi.org/10.1016/j. bbrc.2011.04.087

Ly JD, Grubb DR, Lawen A. Mitochondrial membrane potential (ψ) in apoptosis; an update. Apoptosis. 2003 Mar; 8(2):115–28. PMid: 12766472. https://doi. org/10.1023/A:1022945107762