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Tytuł pozycji:

The Effects of Incensole Acetate on Neuro-inflammation, Brain-Derived Neurotrophic Factor and Memory Impairment Induced by Lipopolysaccharide in Rats.

Tytuł:
The Effects of Incensole Acetate on Neuro-inflammation, Brain-Derived Neurotrophic Factor and Memory Impairment Induced by Lipopolysaccharide in Rats.
Autorzy:
Marefati N; Department of Physiology and Medical Physics, Faculty of Medicine, Baqiyatallah University of Medical Sciences, Tehran, Iran.
Beheshti F; Neuroscience Research Center, Torbat Heydariyeh University of Medical Sciences, Torbat Heydariyeh, Iran.; Department of Physiology, School of Paramedical Sciences, Torbat Heydariyeh University of Medical Sciences, Torbat Heydariyeh, Iran.
Vafaee F; Neuroscience Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Barabadi M; Student Research Committee, Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Hosseini M; Division of Neurocognitive Sciences, Psychiatry and Behavioral Sciences Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. .; Pharmacological Research Center of Medicinal Plants, Mashhad University of Medical Sciences, Mashhad, Iran. .
Źródło:
Neurochemical research [Neurochem Res] 2021 Sep; Vol. 46 (9), pp. 2473-2484. Date of Electronic Publication: 2021 Jun 26.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Publication: 1999- : New York, NY : Kluwer Academic/Plenum Publishers
Original Publication: New York, Plenum Press
MeSH Terms:
Brain-Derived Neurotrophic Factor/*metabolism
Diterpenes/*therapeutic use
Inflammation/*drug therapy
Memory Disorders/*drug therapy
Neuroprotective Agents/*therapeutic use
Animals ; Anti-Inflammatory Agents/therapeutic use ; Antioxidants/therapeutic use ; Avoidance Learning/drug effects ; Glial Fibrillary Acidic Protein/metabolism ; Hippocampus/drug effects ; Hippocampus/metabolism ; Inflammation/chemically induced ; Inflammation/metabolism ; Lipopolysaccharides ; Memory/drug effects ; Memory Disorders/chemically induced ; Memory Disorders/metabolism ; Morris Water Maze Test/drug effects ; Oxidative Stress/drug effects ; Rats, Wistar
References:
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Contributed Indexing:
Keywords: Brain-derived neurotrophic factor; Incensole acetate; Inflammation; Memory
Substance Nomenclature:
0 (Anti-Inflammatory Agents)
0 (Antioxidants)
0 (Bdnf protein, rat)
0 (Brain-Derived Neurotrophic Factor)
0 (Diterpenes)
0 (GFAP protein, rat)
0 (Glial Fibrillary Acidic Protein)
0 (Lipopolysaccharides)
0 (Neuroprotective Agents)
0 (incensole acetate)
Entry Date(s):
Date Created: 20210626 Date Completed: 20211103 Latest Revision: 20211103
Update Code:
20240105
DOI:
10.1007/s11064-021-03381-3
PMID:
34173963
Czasopismo naukowe
Incensole acetate (IA) is a major component of Boswellia serrata resin that has been shown to have anti-inflammatory, anti-oxidant and neuroprotective properties. The present study determined the effect of IA on lipopolysaccharide (LPS)-induced memory impairment, and hippocampal cytokines and oxidative stress indicators level. We used 32 Wistar rats (220-250 g weight) randomly divided into four groups. The control group, which only received the saline-diluted DMSO (vehicle); LPS group which received LPS and was treated with the vehicle; and two IA-treated groups which received 2.5 or 5 mg/ kg IA before LPS injection. Morris water maze (MWM) and passive avoidance (PA) tests were performed. Finally, the brains were removed and were used to assess cytokines levels and oxidative stress status. Compared to the LPS group, IA administration reduced the time spent and path traveled to reach the hidden platform during 5 days of learning in MWM while increased the time spent in the target quadrant in the probe test. Moreover, IA increased latency while decreased entry number and time spent in the dark chamber of PA test compared to the LPS group. Additionally, pre-treatment with IA attenuated interleukin(IL)-6, tumor necrosis alpha (TNF-α), glial fibrillary acidic protein (GFAP), malondialdehyde (MDA) and nitric oxide (NO) metabolites levels while increased those of IL-10, total thiol, superoxide dismutase (SOD), catalase (CAT) and brain-derived neurotrophic factor (BDNF). Our results indicated that IA improved LPS-induced learning and memory impairments. The observed effects seem to be mediated via a protective activity against neuro-inflammation and brain tissue oxidative damage and through improving BDNF.
(© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

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