Format

Send to

Choose Destination
Nutrients. 2017 Jan 3;9(1). pii: E24. doi: 10.3390/nu9010024.

Neuroprotective Effects of Aged Garlic Extract on Cognitive Dysfunction and Neuroinflammation Induced by β-Amyloid in Rats.

Author information

1
Department of Anatomy, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand. nutchareeporn16@gmail.com.
2
Center for Research and Development of Herbal Health Products, Khon Kaen University, Khon Kaen 40002, Thailand. nutchareeporn16@gmail.com.
3
Department of Anatomy, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand. wankun@kku.ac.th.
4
Center for Research and Development of Herbal Health Products, Khon Kaen University, Khon Kaen 40002, Thailand. wankun@kku.ac.th.
5
Department of Anatomy, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand. jariya@kku.ac.th.
6
Center for Research and Development of Herbal Health Products, Khon Kaen University, Khon Kaen 40002, Thailand. jariya@kku.ac.th.
7
Neuroscience Research and Development Group, Khon Kaen University, Khon Kaen 40002, Thailand. jariya@kku.ac.th.
8
Department of Anatomy, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand. cwunnee@kku.ac.th.
9
Department of Anatomy, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand. skitti@kku.ac.th.
10
Center for Research and Development of Herbal Health Products, Khon Kaen University, Khon Kaen 40002, Thailand. skitti@kku.ac.th.
11
Center for Research and Development of Herbal Health Products, Khon Kaen University, Khon Kaen 40002, Thailand. bungorn@kku.ac.th.

Abstract

Neuroinflammation is pathological evidence of Alzheimer's disease (AD) that likely starts as a host defense response to the damaging effects of the β-amyloid (Aβ) deposits in the brain. The activation of microglia may promote the neurodegenerative process through the release of proinflammatory cytokines, such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNFα), which may lead to neuronal damage and eventual death. Aged garlic extract (AGE) has been reported to have multiple biological activities, including anti-inflammatory effects. Therefore, the objective of this study was to investigate the effect of AGE on Aβ (1-42)-induced cognitive dysfunction and neuroinflammation. Adult male Wistar rats were given AGE (125, 250, and 500 mg/kg BW, body weight), orally administered, daily for 56 days. They were then injected with 1 μL of aggregated Aβ (1-42) into the lateral ventricles; bilaterally. Seven days later, their recognition memory was evaluated using a novel object recognition (NOR) test. Then the rats were sacrificed to investigate the alteration of microglia cells, IL-1β and TNFα in the cerebral cortex and hippocampus. The results indicated that AGE at doses of 250 and 500 mg/kg BW significantly improved short-term recognition memory in cognitively impaired rats. In addition, AGE significantly minimized the inflammatory response by reducing the activation of microglia and IL-1β to the levels found in the control, which is similar to the results found in Celebrex-treated rats. In conclusion, AGE may be useful for improving the short-term recognition memory and relieve the neuroinflammation in Aβ-induced rats.

KEYWORDS:

Alzheimer’s disease; aged garlic extract; neuroinflammation; neuroprotection; object recognition; β-amyloid

PMID:
28054940
PMCID:
PMC5295068
DOI:
10.3390/nu9010024
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Multidisciplinary Digital Publishing Institute (MDPI) Icon for PubMed Central
Loading ...
Support Center