Impaired NF-κB/Nrf2 Crosstalk in Rett Syndrome.
Cordone V, Vallese A, Bianchi A, Guiotto A, Pecorelli A
Medicinal Plants
Sulforaphane, the compound that makes broccoli and other brassicas bitter, is emerging as a genuine therapeutic agent in human disease research — not just a talking point on a wellness blog.
Our bodies use two teams of proteins to handle stress: one fights inflammation, and the other neutralizes harmful molecules called free radicals. In Rett syndrome, these two teams stop communicating — the inflammation team runs unchecked while the cleanup team sits idle. Scientists found that using sulforaphane (from broccoli) together with an inflammation-blocking drug could partially get these teams working together again, at least in skin cells grown in a dish.
Key Findings
RTT patient cells showed elevated nuclear NF-κB p65 and increased acetylated NF-κB at baseline, indicating constitutive inflammatory activation without a proportional antioxidant (Nrf2) response.
When challenged with LPS (a bacterial stimulus), RTT fibroblasts failed to activate either the NF-κB or Nrf2 pathway, showing blunted transcriptional responses compared to healthy controls.
Combined treatment with sulforaphane (Nrf2 activator) and BAY-117082 (NF-κB inhibitor) significantly reduced pro-inflammatory cytokine expression and increased HMOX1/HO-1 antioxidant gene expression in RTT cells.
chevron_right Technical Summary
Researchers found that cells from people with Rett syndrome — a rare neurological disorder — are stuck in a state of chronic inflammation because two key protective pathways fail to work together properly. Combining an anti-inflammatory drug with a natural compound found in broccoli (sulforaphane) partially corrected this imbalance in lab-grown cells.
Abstract Preview
Rett syndrome (RTT), caused primarily by mutations in the X-linked MECP2 gene, is a neurodevelopmental disorder marked by systemic alterations, including mitochondrial dysfunction, chronic oxidativ...
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