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Merck

Cognitive effects of vanillic acid against streptozotocin-induced neurodegeneration in mice.

Pharmaceutical biology (2014-12-05)
Jayasingh Chellammal Hanish Singh, Rahul Motiram Kakalij, Rahul Padmakar Kshirsagar, Boyina Hemanth Kumar, Sai Santosh Babu Komakula, Prakash Vamanrao Diwan
RÉSUMÉ

Vanillic acid (VA), a flavoring agent used in food and drug products, obtained naturally from the plant Angelica sinensis (Oliv.) Diels (Apiaceae), used in the traditional Chinese medicine. It is reported to possess strong antioxidant, anti-inflammatory, and neuroprotective effects. However, the pharmacological effects on oxidative stress-induced neurodegeneration are not well investigated. This study investigates the neuroprotective effect of VA on streptozotocin (STZ)-induced neurodegeneration in mice through behavioral and biochemical parameters. The behavioral effects were determined using the Y-maze and open-field habituation memory. In biochemical parameters, acetylcholinesterase (AChE), corticosterone, tumor necrosis factor (TNF)-α, and antioxidants (superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase) were measured. Five groups of animals used were of control, negative control, and three separate groups treated with 25, 50, and 100 mg/kg of VA, respectively, for 28 d. Intracerebroventricular (ICV) injections of STZ were performed for all groups except control on 14th and 16th of 28 d of VA treatment. VA improved spatial learning and memory retention by preventing oxidative stress compared with control animals. VA at 50 and 100 mg/kg dose significantly (p < 0.001) improved the habituation memory, decreased the AChE, corticosterone, TNF-α, and increased the antioxidants (p < 0.001). VA (100 mg/kg) exhibited dose-dependent effect in all parameters with p < 0.001 except antioxidants in which VA showed the significance of p < 0.01. VA exhibited reduction in AChE, TNF-α, and corticosterone with improved antioxidants to contribute neuroprotection and could be an effective therapeutic agent for treating neurodegenerative disorders.

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