American Journal of Chinese Medicine 2015-01-01

Artemisia capillaris Thunberg Produces Sedative-Hypnotic Effects in Mice, Which are Probably Mediated Through Potentiation of the GABAA Receptor.

Jiangyuan Hu, Samuel Schacher

Index: Am. J. Chin. Med. 43 , 667-79, (2015)

Full Text: HTML

Abstract

The Artemisia group of plants has long been used as a traditional remedy for various conditions. The present study assessed the sleep-promoting (sedative-hypnotic) effects of Artemisia capillaris Thunberg (A. capillaris), and elucidated a possible mechanism behind its effect. ICR mice were given A. capillaris extract (oral) at different dosages (50, 100, 200, 300, or 400 mg/kg), distilled water (oral; control), or diazepam (intraperitoneal; reference drug). One hour after administration, locomotion (open-field test) and motor coordination (rota-rod test) were assessed. The extract's effect on pentobarbital-induced sleep was also evaluated. Additionally, electroencephalographic (EEG) recordings were measured in rats. To evaluate a possible mechanism behind its effects, changes in chloride ( Cl (-)) ion influx were measured in human neuroblastoma cells. As compared to the control group, mice treated with A. capillaris demonstrated significantly decreased locomotor activity and impaired motor balance and coordination. The extract also shortened the onset and lengthened the duration of sleep induced by pentobarbital sodium. These effects were comparable to that induced by diazepam. Furthermore, A. capillaris-treated rats showed increased delta and decreased alpha EEG waves; an electroencephalographic pattern indicative of relaxation or sedation. In neuroblastoma cells, the extract dose-dependently increased Cl (-) ion influx, which was blocked by co-administration of bicuculline, a GABAA receptor competitive antagonist, suggesting that its effects are mediated through the GABAA receptor- Cl (-) ion channel complex. Altogether, the results of the present study demonstrate that A. capillaris possesses potent sedative-hypnotic effects, which are probably mediated through potentiation of the GABAA receptor- Cl (-) ion channel complex.