Abstract
Traumatic brain injury (TBI) is a severe condition that leads to brain damage and affects brain function. Importantly, TBI incurs public health costs due to its high mortality, and effective treatment for TBI is still lacking. Docosahexaenoic acid (DHA) has a neuroprotective effect that can reduce oxidative, apoptosis, and inflammatory processes. Administration of DHA after TBI attenuates oxidative stress and protein accumulation and is regarded as a potential therapeutic. Iduna is a regulator of parthanatos, and upregulation of Iduna reduces cellular damage and mitochondrial dysfunction. Thus, we speculated that overexpression of Iduna might promote DHA therapy in the treatment of TBI. Here, we found that after combination overexpression of Iduna and DHA in a mouse model of TBI, the expression of inflammatory factors was reduced, while the secretion of neuroprotective factors was increased. In addition, we found that these effects might be mediated by the Wnt/MDM2 pathway, and Iduna might be a therapeutic target for TBI.