ArticleFrontiers in nutrition2025
Oolong tea attenuates neuroinflammation by modulating the microbiota-gut-brain axis in a rat model of autism.
Article in Frontiers in nutrition, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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- Genome-Wide Identification and Expression Analysis of theCurrent issues in molecular biology · 2026Article
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Abstract
Background: Autism spectrum disorder (ASD) is a prevalent neurodevelopmental disorder with limited effective treatments. Emerging evidence implicates dysregulation of the microbiota-gut-brain axis in ASD pathogenesis. Oolong tea (OT), a traditional Chinese tea with neuroprotective properties, may modulate this axis, but its effects and mechanisms in ASD remain unclear. We investigated whether OT attenuates neuroinflammation in a valproic acid (VPA)-induced rat model of autism through the microbiota-gut-brain axis and the TLR-4/IκB-α/NF-κB signaling pathway. Methods: An ASD model was established by prenatal VPA exposure (500 mg/kg, i.p., E12.5). Postnatal VPA-treated rats received OT (100, 200, or 400 mg/kg/day) for 4 weeks. Behavioral assessments included self-grooming, marble burying, and three-chamber social interaction tests. Nissl staining evaluated neuropathology. Gut microbiota composition was analyzed using 16S rRNA sequencing of fecal samples. Lipopolysaccharide (LPS), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) levels were measured in the plasma, intestine, and brain using enzyme-linked immunosorbent assay. Intestinal and blood-brain barrier (BBB) integrity (claudin-1/5, occludin, ZO-1) and TLR-4/IκB-α/NF-κB pathway activation were assessed by Western blot/immunofluorescence. Microglial (Iba-1) and astrocytic (GFAP) activation and neuronal TLR-4 localization (co-staining with Neun) were examined. Antibiotic cocktail (ABX)-induced microbiota depletion validated gut microbiota dependency. Results: OT (400 mg/kg/day) significantly ameliorated repetitive behaviors (reduced self-grooming duration and marble burying), sociability deficits (improved sociability/social preference index), and attenuated cortical neuronal loss in VPA-treated rats. OT restored gut microbiota dysbiosis, specifically reducing pathogenic Conclusion: OT attenuates ASD-like phenotypes and neuroinflammation in VPA-treated rats by rebalancing gut microbiota, restoring intestinal/BBB barriers, and inhibiting neuronal TLR-4/IκB-α/NF-κB signaling. This study highlights OT's potential as a microbiota-targeted therapeutic strategy for ASD.
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