Validation experiment designed to validate causal mechanisms targeting N/A in mice. Primary outcome: anxiety- and depression-like behaviors
This comprehensive animal study investigated the neuroprotective effects of lycopene (Lyc) against di(2-ethylhexyl) phthalate (DEHP)-induced neurotoxicity in mice over 35 consecutive days. The experiment utilized a multi-faceted approach combining behavioral assessments, molecular biology analyses, transcriptomics, and microbiome profiling to understand the gut-brain axis mechanisms. Mice received daily intragastric administrations of either DEHP (to induce neurotoxicity) or Lyc (as treatment). The study evaluated anxiety- and depression-like behaviors, neuroinflammation in the hippocampus, gut microbiota composition, intestinal barrier integrity, and inflammatory signaling pathways. Key findings showed that Lyc administration effectively ameliorated DEHP-induced behavioral deficits, reduced hippocampal neuroinflammation through modulation of NOD-like receptor signaling, improved gut microbiota by promoting beneficial bacteria like Akkermansiaceae, enhanced intestinal barrier function via increased tight junction proteins, and regulated LPS-TLR4/MyD88 signaling in the colon to reduce local inflammation.
Daily intragastric administration of DEHP or Lyc for 35 consecutive days, followed by behavioral testing, transcriptome analysis, microbiome profiling, and molecular biology assessments
Lycopene would protect against DEHP-induced neurotoxicity through gut-brain axis modulation
Amelioration of DEHP-induced behavioral deficits and neuroinflammation
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