Selenium improves behavioral performance in a rat model of autism spectrum disorder by mitigating oxidative stress and modulating the Sirt1/Keap1/Nrf2/HO-1 signaling pathway.

Researchers studied selenium supplements in rats with autism-like behaviors. The rats were given selenium and showed better behavior, less brain inflammation, and healthier brain cells. Selenium worked by activating protective pathways in the brain that fight harmful molecules. While promising, this was only tested in animals, so we don't know if selenium would help autistic children.

This preclinical study investigated selenium supplementation in a rat model of autism spectrum disorder (ASD) induced by valproic acid during pregnancy. Rats treated with sodium selenite showed improved behavioral performance, reduced oxidative stress and inflammation, and preserved neuronal structure in hippocampal tissues. The protective effects were associated with modulation of the Sirt1/Keap1/Nrf2/HO-1 signaling pathway, with selenium treatment upregulating beneficial proteins (Sirt1, Nrf2, HO-1) while downregulating harmful ones (Keap1). The study used behavioral assessments, morphological evaluations, and molecular analyses to demonstrate selenium's neuroprotective properties through antioxidant and anti-inflammatory mechanisms.

While selenium shows promise as a neuroprotective intervention for autism through antioxidant mechanisms, this remains preliminary animal research. Human clinical trials are needed before recommending selenium supplementation for autistic individuals. Current findings support further investigation of selenium's role in autism treatment.

Animal model study only; unclear sample size; valproic acid model may not fully represent human autism; no long-term follow-up; unclear optimal dosing; requires human studies to confirm safety and efficacy.

Autism spectrum disorder (ASD) is a diverse collection of neurodevelopmental disorders often accompanied by excessive oxidative stress and chronic inflammatory responses. Selenium (Se), a trace element, has demonstrated anti-inflammatory, antioxidant, and neuroprotective effects. The present study aimed to examine the effects of sodium selenite, a Se supplement, on a rat model of ASD. The valproic acid intervention method was used during pregnancy to construct an ASD rat model.

Rats were then treated with sodium selenite. Behavioral tests, morphological assessments, and measurements of antioxidant enzymes, oxidative stress indicators, and inflammatory factors in the hippocampal tissues and serum were conducted. Se supplementation mitigated inflammatory responses and oxidative stress in ASD rats while preserving neuronal morphology and function. In addition to Se supplementation, rats received specific inhibitors targeting the signaling pathway.

Protein and mRNA expression levels, as well as the tissue distribution of sirtuin 1 (Sirt1), heme oxygenase-1 (HO-1), nuclear factor erythroid 2-related factor 2 (Nrf2), and Kelch-like ECH-associated protein 1 (Keap1), were evaluated. The results demonstrated that Se treatment upregulated the expression levels of Sirt1, Nrf2, and HO-1, while downregulating Keap1 expression. These findings demonstrate that Se attenuates inflammatory damage and oxidative stress in the brain, and this protective effect is associated with the Sirt1/Keap1/Nrf2/HO-1 signaling pathway.