Triethylene glycol, an active component of Ashwagandha (Withania somnifera) leaves, is responsible for sleep induction.
Study Design
- Study Type
- In Vitro
- Intervention
- Triethylene glycol, an active component of Ashwagandha (Withania somnifera) leaves, is responsible for sleep induction. 10-30 mg/mouse (triethylene glycol); water extract of Ashwagandha leaves
- Comparator
- Placebo
- Effect Direction
- Positive
- Risk of Bias
- Unclear
Abstract
Insomnia is the most common sleep complaint which occurs due to difficulty in falling asleep or maintaining it. Most of currently available drugs for insomnia develop dependency and/or adverse effects. Hence natural therapies could be an alternative choice of treatment for insomnia. The root or whole plant extract of Ashwagandha (Withania somnifera) has been used to induce sleep in Indian system of traditional home medicine, Ayurveda. However, its active somnogenic components remain unidentified. We investigated the effect of various components of Ashwagandha leaf on sleep regulation by oral administration in mice. We found that the alcoholic extract that contained high amount of active withanolides was ineffective to induce sleep in mice. However, the water extract which contain triethylene glycol as a major component induced significant amount of non-rapid eye movement sleep with slight change in rapid eye movement sleep. Commercially available triethylene glycol also increased non-rapid eye movement sleep in mice in a dose-dependent (10-30 mg/mouse) manner. These results clearly demonstrated that triethylene glycol is an active sleep-inducing component of Ashwagandha leaves and could potentially be useful for insomnia therapy.
Full Text
Figures
Fig 1
Sleep architecture recordings from mice administered Ashwagandha leaf extract or triethylene glycol (TEG), showing EEG/EMG traces that characterize wake, NREM, and REM sleep states.
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Fig 2
Quantitative sleep stage analysis comparing triethylene glycol-treated mice to vehicle controls, with time spent in NREM sleep significantly increased following TEG administration.
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Fig 3
Dose-response data for triethylene glycol's somnogenic effects, demonstrating concentration-dependent increases in non-rapid eye movement sleep duration in mice.
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Fig 4
Circadian sleep pattern analysis following Ashwagandha-derived triethylene glycol administration, showing the temporal distribution of sleep promotion across light and dark phases.
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