期刊
NEUROCHEMISTRY INTERNATIONAL
卷 143, 期 -, 页码 -出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuint.2020.104899
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Silexan (R), a proprietary essential oil from Lavandula angustifolia flowers, has been shown to possess anxiolytic and antidepressant effects in patients with anxiety disorders, as well as improving neuroplasticity. Its mechanism of action involves moderate inhibition of voltage dependent calcium channels and activation of intracellular signaling kinases, leading to VDCC modulation and CREB activation.
Silexan (R), a proprietary essential oil manufactured by steam distillation from Lavandula angustifolia flowers showed pronounced anxiolytic effects in patients with subthreshold anxiety disorders and was also efficacious in patients with Generalized Anxiety disorder (GAD). Moreover, evidences for antidepressant-like properties of Silexan (R) have been observed in anxious patients suffering from comorbid depressive symptoms and in patients with mixed anxiety-depression disorder (ICD-10 F41.2). In accordance with the clinical data Silexan (R) is active in several behavioral models in rodents at rather low concentrations indicating potent anxiolytic and antidepressive properties. As possible mechanism of action a moderate inhibition of voltage dependent calcium channels (VDCC) has been found showing some similarities to the anxiolytic drug pregabalin. However, while pregabalin mainly inhibits P/Q-type channels by binding to a modulatory subunit, Silexan (R) moderately inhibits mainly T-type and N-type channels and to some extent P/Q-type channels. Unlike pregabalin Silexan (R) is free of hypnotic or sedative side effects and seems to be devoid of any abuse potential. With respect to its specific antidepressant like properties Silexan (R) improves several aspects of neuroplasticity which seems to be the common final pathway of all antidepressant drugs. As a potential mechanism of its effects on neuroplasticity an activation of the transcription factor CREB via activation of intracellular signaling kinases like PKA and MAPK has been found. Since the concentrations of Silexan (R) needed to inhibit VDCC function and to improve neuroplasticity are quite similar, the effects of Silexan (R) on PKA or MAPK could constitute a common intracellular signaling cascade leading to VDCC modulation as well as CREB activation and improved neuroplasticity.
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