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. 2017:2017:7426538.
doi: 10.1155/2017/7426538. Epub 2017 Apr 26.

The Protective Effect of Lavender Essential Oil and Its Main Component Linalool against the Cognitive Deficits Induced by D-Galactose and Aluminum Trichloride in Mice

Affiliations

The Protective Effect of Lavender Essential Oil and Its Main Component Linalool against the Cognitive Deficits Induced by D-Galactose and Aluminum Trichloride in Mice

Pan Xu et al. Evid Based Complement Alternat Med. 2017.

Abstract

Lavender essential oil (LO) is a traditional medicine used for the treatment of Alzheimer's disease (AD). It was extracted from Lavandula angustifolia Mill. This study was designed to investigate the effects of lavender essential oil (LO) and its active component, linalool (LI), against cognitive impairment induced by D-galactose (D-gal) and AlCl3 in mice and to explore the related mechanisms. Our results revealed that LO (100 mg/kg) or LI (100 mg/kg) significantly protected the cognitive impairments as assessed by the Morris water maze test and step-though test. The mechanisms study demonstrated that LO and LI significantly protected the decreased activity of superoxide dismutase (SOD), glutathione peroxidase (GPX), and protected the increased activity of acetylcholinesterase (AChE) and content of malondialdehyde (MDA). Besides, they protected the suppressed nuclear factor-erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) expression significantly. Moreover, the decreased expression of synapse plasticity-related proteins, calcium-calmodulin-dependent protein kinase II (CaMKII), p-CaMKII, brain-derived neurotrophic factor (BDNF), and TrkB in the hippocampus were increased with drug treatment. In conclusion, LO and its active component LI have protected the oxidative stress, activity of cholinergic function and expression of proteins of Nrf2/HO-1 pathway, and synaptic plasticity. It suggest that LO, especially LI, could be a potential agent for improving cognitive impairment in AD.

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Conflict of interest statement

Authors have no conflict of interests in this study.

Figures

Figure 1
Figure 1
Molecular structure of linalool.
Figure 2
Figure 2
Effect of LO and LI on the total distance travelled in open-field test. Data are expressed as means ± SEM. n = 12-13 in each group.
Figure 3
Figure 3
Effect of LO and LI on D-gal and AlCl3 induced cognitive deficits in MWM test. Latency to find platform (a) and escape rate (b) were measured for 5-day navigation. Swimming distance in the target quadrant (c) and crossing number (d) were recorded during the probe trial. Values are presented as mean ± SEM (n = 12 in each group). #P < 0.05, compared with the control group, and P < 0.05 compared with the D-gal and AlCl3 treated group.
Figure 4
Figure 4
Effect of LO and LI on D-gal and AlCl3 induced cognitive deficit in step-through tests. Latency into dark chamber (a) and error times (b) were detected in consolidation trial. Data are shown as mean ± SEM (n = 12 in each group). #P < 0.05 compared with the control group and P < 0.05 compared with the D-gal and AlCl3 treated group.
Figure 5
Figure 5
Effects of LO and LI on levels of Nrf2 and HO-1 in mice hippocampus. Mice were grouped and treated as described in the text. (a) The expressions of Nrf2 and HO-1 were measured by Western blot. (b) Quantitative analysis of bands density. The ratio to β-actin was calculated (n = 3 per group). Values are shown as mean ± SEM. #P < 0.05 compared with control group and P < 0.05 compared with D-gal and AlCl3 treated group.
Figure 6
Figure 6
Effects of LO and LI on levels of BDNF and TrkB in mice hippocampus. Mice were grouped and treated as described in the text. The expressions of (a) CaMKII and p-CaMKII and (c) BDNF and TrkB were measured by Western blot. (b) and (d) Quantitative analysis of bands density. The ratio to β-actin was calculated (n = 3 per group). Values are shown as mean ± SEM. #P < 0.05 compared with control group and P < 0.05 compared with D-gal and AlCl3 treated group.

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References

    1. Dunne T. E. Alzheimer's disease: an overview. In: Friedman H. S., editor. Encyclopedia of Mental Health. 2nd. Oxford, UK: Academic Press; 2016. pp. 58–63.
    1. Stuchlik A. Dynamic learning and memory, synaptic plasticity and neurogenesis: an update. Frontiers in Behavioral Neuroscience. 2014;8, article 106 doi: 10.3389/fnbeh.2014.00106. - DOI - PMC - PubMed
    1. Pang P. T., Lu B. Regulation of late-phase LTP and long-term memory in normal and aging hippocampus: role of secreted proteins tPA and BDNF. Ageing Research Reviews. 2004;3(4):407–430. doi: 10.1016/j.arr.2004.07.002. - DOI - PubMed
    1. Peng X.-M., Gao L., Huo S.-X., Liu X.-M., Yan M. The mechanism of memory enhancement of acteoside (verbascoside) in the senescent mouse model induced by a combination of D-gal and AlCl3. Phytotherapy Research. 2015;29(8):1137–1144. doi: 10.1002/ptr.5358. - DOI - PubMed
    1. Li Z., Zhao G., Qian S., et al. Cerebrovascular protection of β-asarone in Alzheimer's disease rats: a behavioral, cerebral blood flow, biochemical and genic study. Journal of Ethnopharmacology. 2012;144(2):305–312. doi: 10.1016/j.jep.2012.09.013. - DOI - PubMed

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