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Updated: May 4, 2026
Meta-Analysis of the Effectiveness and Safety of Shugan Jieyu Capsules for the Treatment of Insomnia
Published on: February 17, 2023
Tianwang Buxin Decoction ameliorates neuroinflammation in insomnia via adenosine accumulation-mediated AMPK/SIRT1
Yaqi Li1, Shiyu Ji1, Jiecheng Jiang1
1Hubei University of Chinese Medicine, Basic Medical College, Wuhan, Hubei, 430070, China; Engineering Research Center of TCM Protection Technology and New Product Development for the Elderly Brain Health, Ministry of Education, Wuhan, Hubei, 430070, China.
Ethnopharmacological Relevance:
Adenosine (Ado) is a key signaling molecule in the central nervous system. Under cellular stress, extracellular Ado accumulation drives neuroinflammation-induced neuronal damage and sleep dysfunction. Tianwang Buxin Decoction (TWBXD) demonstrates long-term therapeutic efficacy for insomnia. However, the related pharmacological pathways require further mechanistic studies.
Aim Of The Study:
To elucidate the therapeutic effects of TWBXD against insomnia and its mechanisms in mitigating Ado-induced neuroinflammation.
Materials And Methods:
TWBXD components were analyzed using liquid chromatography-tandem mass spectrometry (LC-MS/MS). An in vivo insomnia model was established by inducing adenosine A2A receptor (A2aR) overexpression in the basal forebrain. Sleep architecture was monitored via 24-h polysomnography, followed by analyses of histopathology, Ado levels, A2aR expression, inflammatory mediators, and AMPK/SIRT1 activity. In vitro, neuroinflammation was modeled in a neuron-astrocyte co-culture using A2aR-overexpressing plasmids. TWBXD-containing serum effects on cell viability, Ado dynamics, and inflammatory responses were assessed.
Results:
Ado accumulation induced neuroinflammation and disrupted sleep. TWBXD exhibited optimal efficacy at 17.6 g/kg compared with other doses. It reversed Ado-mediated suppression of the AMP-activated protein kinase (AMPK)/Sirtuin 1 (SIRT1) axis to improve sleep architecture, inhibiting the expression of downstream pro-inflammatory mediators such as nuclear factor-κB, interferon-γ, and interleukin-1β while promoting that of interleukin-10. In vitro experiments and molecular docking verified that TWBXD's neuroprotective effects against Ado overload are mediated by functional A2aR antagonism.
Conclusion:
Neuroinflammation in insomnia is promoted by Ado-driven suppression of the AMPK/SIRT1 signaling pathway. TWBXD restores this axis to alleviate insomnia, representing a novel therapeutic strategy for managing neuroinflammation-related sleep disorders.
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