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

Abstract

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 (220-250g 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 5mg/ 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 5days 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.