ArticleJournal of advanced research2025
Astragaloside IV ameliorates autism-like behaviors in BTBR mice by modulating Camk2n2-dependent OXPHOS and neurotransmission in the mPFC.
Article in Journal of advanced research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Genetic and pharmacological evidence linking CB1R signaling to hippocampal GABAergic dysfunction in ASD mouse model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- ASIV Attenuates Cisplatin-Induced Proximal Tubular Injury by Enhancing Mitochondrial Biogenesis and Mitophagy Through the ADRA1A/AMPK/FOXO3A Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Astragaloside IV mitigates mitochondrial damage and neurological symptoms in rats with cervical spondylotic myelopathy by inhibiting IL-17/TRAF6/NF-κB pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Article
- Ertugliflozin improves animal behaviours associated with oxidative stress and inflammation in a BTBRBrain communications · 2026Article
- The effects of traditional Chinese botanical medicine on membranous nephropathy.Frontiers in pharmacology · 2026Review
- Naringin Alleviates Autistic-Like Behaviors in BTBR Mice Through Cannabinoid Receptor Type 1-Mediated Restoration of Hippocampal Neurogenesis.CNS neuroscience & therapeutics · 2025Article
- The Role of GABA Pathway Components in Pathogenesis of Neurodevelopmental Disorders.International journal of molecular sciences · 2025Review
- Oxytocin enhances oligodendrocyte development and improves social deficits in autistic rats.Frontiers in neuroscience · 2025Article
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11 authors.
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Abstract
introductionAutism spectrum disorder (ASD) represents a multifaceted set of neurodevelopmental conditions marked by social deficits and repetitive behaviors. Astragaloside IV (ASIV), a natural compound derived from the traditional Chinese herb Astragali Radix, exhibits robust neuroprotective effects. However, whether ASIV can ameliorate behavioral deficits in ASD remains unknown.
objectivesThis work aimed to determine the efficacy and molecular mechanisms of ASIV in ASD.
methodsThe autistic BTBR T + tf/J (BTBR) mice were used in this study. Behavioral tests were performed to assess the ASD-like phenotypes. The neurotransmitter levels and synaptic transmission were evaluated by high-performance liquid chromatography and whole-cell patch clamp recordings, respectively. Molecular biological techniques, immunostaining, and RNA-sequencing (RNA-seq) were combined to uncover the underlying molecular mechanisms.
resultsOur study showed that both social impairment and repetitive behaviors were significantly improved after ASIV treatment in a dose-dependent manner in BTBR mice. The ASIV treatment normalized the neurotransmitter levels (GABA and glutamate) and their corresponding vesicular transporters (vGAT, vGLUT1) in the medial prefrontal cortex (mPFC). Furthermore, the excitation-inhibition imbalance in layer V of mPFC was reversed after ASIV administration. Mechanistically, bulk RNA-seq and PPI network analysis identified Camk2n2 as the crucial bridging gene regulating oxidative phosphorylation and neurotransmission. Camk2n2 overexpression in the mPFC abolished the beneficial effects of ASIV on autistic symptoms in BTBR mice via the Camk2/CREB pathway.
conclusionThe evidence demonstrates that ASIV may become a promising treatment option for ASD and implies that targeting the Camk2n2/Camk2/CREB axis is warranted to investigate these ASD individuals further.
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