Minocycline improves the recovery of nerve function and alleviates blood-brain barrier damage by inhibiting endoplasmic reticulum in traumatic brain injury mice model

Traumatic brain injury (TBI) is a clinical emergency with very high incidence, disability, and fatality rate. Minocycline, widely used semisynthetic second-generation tetracycline antibiotic, has anti-inflammatory bactericidal effects. However, minocycline not been explored as therapeutic drug in TBI if effective, the related molecular mechanism also unclear. In this study, we examined neuroprotective effect possible of minocycline, mice model by studying trauma-related functional morphological changes. Also, vitro cell studies were carried out to verify animal data. We found that significantly improved neurobehavioral score, inhibited apoptosis, repaired blood-brain barrier, reduced levels inflammatory factors Interleukin-6 tumor necrosis factor-α mice. vitro, upon oxygen glucose deprivation, cellular increased tight junction adherens proteins, thereby improving viability. Moreover, Mino treatment prevented loss proteins which markedly reversed an ER stress activator (tunicamycin) both vivo vitro. Our findings set effective basis for use treat injury-induced neurological deficits.