Taurine supplementation reduces neuroinflammation and protects against white matter injury after intracerebral hemorrhage in rats

Intracerebral hemorrhage (ICH) initiates a neuroinflammatory cascade that contributes to substantial neuronal damage and neurological deterioration. Taurine, an abundant amino acid in the nervous system, is reported to reduce inflammatory injury in various central nervous system diseases, but its role and the possible underlying mechanisms in the pathology following ICH remains unclear. This study was designed to evaluate the effect of taurine supplementation on neurological deficits, acute inflammatory responses and white matter injury in a model of ICH in rats. Adult male Sprague-Dawley (SD) rats subjected to collagenase-induced ICH injury were injected intravenously with different concentrations of taurine or vehicle 10 min after ICH and subsequently daily for 3 days. Behavioral studies, brain water content, and assessments of hemorrhagic lesion volume were quantified at day 1 and day 3 post-ICH. Neuronal damage, peri-hematomal inflammatory responses, and white matter injury were determined at 24 h, meanwhile, the content of hydrogen sulfide (H2S) along with the expression of cystathionine-beta-synthase (CBS) and P2X7 receptor (P2X7R) in peri-hematomal tissues was analyzed to investigate the possible anti-inflammatory mechanism of taurine. Treatment with a high dosage of taurine (50 mg/kg) significantly attenuated functional deficits and reduced brain edema and hemorrhagic lesion volume after ICH. Taurine administration also resulted in significant amelioration of neuronal damage and white matter injury. These changes were associated with marked reductions in neutrophil infiltration, glial activation, and expression levels of inflammatory mediators. Moreover, the anti-inflammatory effect of taurine was accompanied by increased H2S content, enhanced CBS expression, and less expression of P2X7R. Our study demonstrated that the high dosage of taurine supplementation effectively mitigated the severity of pathological inflammation and white matter injury after ICH, and the mechanism may be related to upregulation of H2S content and reduced P2X7R expression.