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

Neurochemical Research - Tập 46 - Trang 2473-2484 - 2021
Narges Marefati1, Farimah Beheshti2,3, Farzaneh Vafaee4, Moslem Barabadi5, Mahmoud Hosseini6,7
1Department of Physiology and Medical Physics, Faculty of Medicine, Baqiyatallah University of Medical Sciences, Tehran, Iran
2Neuroscience Research Center, Torbat Heydariyeh University of Medical Sciences, Torbat Heydariyeh, Iran
3Department of Physiology, School of Paramedical Sciences, Torbat Heydariyeh University of Medical Sciences, Torbat Heydariyeh, Iran
4Neuroscience research Center, Mashhad University of Medical Sciences, Mashhad, Iran
5Student Research Committee, Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
6Division of Neurocognitive Sciences, Psychiatry and Behavioral Sciences Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
7Pharmacological Research Center of Medicinal Plants, Mashhad University of Medical Sciences, Mashhad, Iran

Tóm tắt

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.

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