Mechanism of essential oil of Ligusticum chuanxiong to prevent and treat vascular cognitive impairment induced by lipopolysaccharide in mice / 中草药

ABSTRACT

Objective: To explore the effect of volatile oil of Ligusticum chuanxiong on vascular cognitive impairment (VCI) induced by lipopolysaccharide (LPS) and its related mechanism. Methods Male C57BL/C mice were randomly divided into sham-operated group, model group, memantine (10 mg/kg) group, and volatile oil of L. chuanxiong (30, 15, and 7.5 mg/kg) groups, drugs were given by ig administration once a day for 14 d. On day 8, LPS was injected into the lateral ventricle in mice. On day 11 and day 12, the cognitive ability were checked by the Y maze and step down test. On day 15 the mice were decapitated and the brain tissue was taken to determine the levels of monoamine oxidase (MAO), acetylcholinesterase (AchE), and acetylcholine (Ach); At the same time, the effect of the drug on superoxide dismutase (SOD) in mitochondria of brain in SD rats and the activity of Ec AchE, and BV-2 cells of microgliomas injured by LPS were also investigated in vitro. Results:LPS significantly increased the levels of MAO and AchE in the brain in mice, while decreased the levels of dopamine (DA), 5-hydroxytryptamine (5-HT), and norepinephrine (NE). The volatile oil of L. chuanxiong 30 or 15 mg/kg decreased the level of MAO and AchE in the brain of LPS mice. The volatile oil of L. Chuanxiong could significantly increase the times of spontaneous alternation reaction in Y maze in VCI mice, and the middle dose could significantly decrease the latency of VCI mice in step down test. In vitro, the volatile oil of L. chuanxiong 1 mg/mL had a weak inhibitory effect on AchE of electric eel. The volatile oil of L. chuanxiong 0.5 μg/mL could significantly increase the activity of SOD in brain mitochondria of rats, and decrease the levels of tumor necrosis factor-α (TNF-α) and nitric oxide (NO) increased significantly in BV-2 cells induced by LPS. Conclusion: The volatile oil of L. chuanxiong can significantly improve the cognitive ability of VCI induced by LPS in mice, and its mechanism may be related to inhibit the inflammatory response in the brain and alleviate the injury of neurons.