Enriched environment attenuates ferroptosis after cerebral ischemia/reperfusion injury by regulating iron metabolism

This study aims to explore the potential molecular mechanisms by which EE modulates iron metabolism to reduce ferroptosis. The experimental animals were randomly divided into four groups based on the housing environment and the procedure the animals received: the sham-operated + standard environment (SSE) group, the sham-operated + enriched environment (SEE) group, the ischemia/reperfusion + standard environment (ISE) group, and the ischemia/reperfusion + enriched environment (IEE) group. The results showed that EE reduced IL-6 expression during cerebral I/R injury, hence reducing JAK2-STAT3 pathway activation and hepcidin expression. Reduced hepcidin expression led to decreased DMT1 expression and increased FPN1 expression in neurons, resulting in lower neuronal iron levels and alleviated ferroptosis. In addition, EE also reduced the expression of TfR1 in neurons. Our research suggested that EE played a neuroprotective role by modulating iron metabolism and reducing neuronal ferroptosis after cerebral I/R injury, which might be achieved by inhibiting inflammatory response and down-regulating hepcidin expression.PMID:37812906 | DOI:10.1016/j.brainresbull.2023.110778
Source: Brain Research Bulletin - Category: Neurology Authors: Source Type: research