From brain to body: sinapic acid prevents multi-organ damage post-traumatic brain injury in mice.

Traumatic Brain Injury (TBI) is a critical neurological condition that severely affects the brain and extracranial organs. Secondary damages such as BBB disruption, oxidative stress, and inflammation in the brain can induce systemic pathophysiological changes in multiple organs, primarily in the heart, lungs, liver, and kidneys, known as Multiple Organ Dysfunction Syndrome (MODS). Systemic hyperinflammation, autonomic dysfunction, and immunosuppression collectively play a crucial role in the progression of MODS. The current study aimed to investigate the therapeutic efficacy of the polyphenolic compound, sinapic acid (SA), against this complex disease. The Weight Drop model was used to induce TBI in Swiss albino mice, which were divided into four groups: control, TBI, SA 30, and SA 50. SA was administered orally to the test groups at doses of 30 mg/kg and 50 mg/kg for 21 days post-injury. Several behavioural, biochemical, molecular, and histopathological parameters were assessed at days 1 and 21 post-injury. The results highlighted that SA treatment significantly improved animal behaviour, restored BBB and lung integrity, reduced oedema, oxidative stress, and inflammation, as well as catecholamine spill. It also restored the normal organ functions, preserved cellular architecture, and upregulated PDL-1 and IL-10 mRNA expression. These findings suggest that SA is a multi-target therapeutic compound having neuroprotective and organoprotective properties, making it a promising candidate that mitigates TBI-induced MODS.