Central nervous system (CNS) injuries are a major cause of neurological impairment and long-term disability, driven by intertwined processes including neuroinflammation, oxidative stress, apoptosis, and disruption of the blood–brain barrier (BBB) or blood–spinal cord barrier (BSCB). This review summarizes the physicochemical features and neuroprotective mechanisms of tanshinone IIA (TanIIA), a lipophilic diterpene quinone from Salvia miltiorrhiza , and appraises preclinical evidence across CNS injury models. By synthesizing recent experimental findings from in vivo and in vitro models of cerebral ischemia and spinal cord injury, we focus on mechanistic pathways and functional outcomes. TanIIA shows BBB permeability and multi-target actions, including suppression of neuroinflammatory signaling, attenuation of oxidative damage, preservation of mitochondrial function, restoration of BBB/BSCB integrity, mitigation of aberrant glial activation, and promotion of neurological recovery. Emerging studies also suggest potential synergy with glucocorticoids, which may allow steroid dose reduction while maintaining efficacy in selected settings. While preclinical results are encouraging, key translational gaps remain, particularly regarding target specificity, pharmacokinetics, formulation, and clinically relevant dosing windows. Future work integrating multi-omics approaches with advanced disease-relevant models may accelerate the development of TanIIA-based therapeutics for CNS injuries.
Guo et al. (Sun,) studied this question.