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Escin attenuates behavioral impairments, oxidative stress and inflammation in a chronic MPTP/probenecid mouse model of Parkinson's disease.

Authors
  • Selvakumar, Govindasamy Pushpavathi1
  • Janakiraman, Udaiyappan1
  • Essa, Musthafa Mohamed2
  • Justin Thenmozhi, Arokiasamy1
  • Manivasagam, Thamilarasan3
  • 1 Department of Biochemistry and Biotechnology, Annamalai University, Annamalainagar 608002, Tamilnadu, India. , (India)
  • 2 Department of Food Science and Nutrition, CAMS, Sultan Qaboos University, Muscat, Oman. , (Oman)
  • 3 Department of Biochemistry and Biotechnology, Annamalai University, Annamalainagar 608002, Tamilnadu, India. Electronic address: [email protected] , (India)
Type
Published Article
Journal
Brain research
Publication Date
Oct 17, 2014
Volume
1585
Pages
23–36
Identifiers
DOI: 10.1016/j.brainres.2014.03.010
PMID: 24657313
Source
Medline
Keywords
License
Unknown

Abstract

Parkinson's disease (PD) is a progressive neurodegenerative disorder that results mainly due to the death of dopaminergic neurons in the substantia nigra (SN), and subsequently has an effect on one's motor function and coordination. The current investigation explored the neuroprotective potential of escin, a natural triterpene-saponin on chronic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine/probenecid (MPTP/p) induced mouse model of PD. Administration of MPTP led to the depleted striatal dopamine content, impaired patterns of behavior, enhanced oxidative stress and diminished expression of tyrosine hydroxylase (TH), dopamine transporter (DAT) and vesicular monoamine transporter-2 (VMAT-2). The expressions of interleukin-6 and -10, glial fibrillary acidic protein (GFAP), ionized calcium-binding adaptor protein-1 (IBA-1), tumor necrosis factor-α (TNF-α) and inducible nitric oxide synthase (iNOS) in SN were also enhanced. Oral treatment of escin significantly attenuated MPTP/p induced dopaminergic markers depletion, physiological abnormalities, oxidative stress and inhibit neuroinflammatory cytokine expressions in SN. The result of our study confirmed that escin mediated its protection against experimental PD through its antioxidant and anti-inflammatory properties.

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