Vanillin Attenuated Behavioural Impairments, Neurochemical Deficts, Oxidative Stress and Apoptosis Against Rotenone Induced Rat Model of Parkinson’s Disease

Chinnasamy Dhanalakshmi, Udaiyappan Janakiraman, Thamilarasan Manivasagam*, Arokiasamy Justin Thenmozhi, Musthafa Mohamed Essa, Ameer Kalandar, Mohammed Abdul Sattar Khan, Gilles J. Guillemin

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

75 Citations (Scopus)

Abstract

Vanillin (4-hydroxy-3-methoxybenzaldehyde), a pleasant smelling organic aromatic compound, is widely used as a flavoring additive in food, beverage, cosmetic and drug industries. It is reported to cross the blood brain barrier and also displayed antioxidant and neuroprotective activities. We previously reported the neuroprotective effect of vanillin against rotenone induced in in vitro model of PD. The present experiment was aimed to analyze the neuroprotective effect of vanillin on the motor and non-motor deficits, neurochemical variables, oxidative, anti-oxidative indices and the expression of apoptotic markers against rotenone induced rat model of Parkinson’s disease (PD). Rotenone treatment exhibited motor and non-motor impairments, neurochemical deficits, oxidative stress and apoptosis, whereas oral administration of vanillin attenuated the above-said indices. However further studies are needed to explore the mitochondrial protective and anti-inflammatory properties of vanillin, as these processes play a vital role in the cause and progression of PD.

Original languageEnglish
Pages (from-to)1899-1910
Number of pages12
JournalNeurochemical Research
Volume41
Issue number8
DOIs
Publication statusPublished - Aug 1 2016

Keywords

  • Motor and non-motor symptoms
  • Oxidative stress, apoptosis
  • Parkinson’s disease
  • Vanillin

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Biochemistry

Fingerprint

Dive into the research topics of 'Vanillin Attenuated Behavioural Impairments, Neurochemical Deficts, Oxidative Stress and Apoptosis Against Rotenone Induced Rat Model of Parkinson’s Disease'. Together they form a unique fingerprint.

Cite this