米诺环素在急性缺血性卒中中的抗神经炎症与脑细胞保护研究进展:从机制到临床证据

Acute ischemic stroke is a major cause of disability and mortality. Despite continuous improvements in reperfusion therapy and secondary prevention strategies, some patients still experience varying degrees of neurological dysfunction after stroke. Neuroinflammation is involved in the onset, progression, and recovery of acute ischemic stroke and has emerged as an important therapeutic target for brain cytoprotection in recent years. Minocycline, a classic tetracycline antibiotic, exerts multiple anti-neuroinflammatory effects beyond its antimicrobial activity, including modulation of microglial activation, suppression of inflammatory cytokine release, inhibition of matrix metalloproteinase activity, and attenuation of peripheral immune-cell infiltration into the central nervous system. Preclinical studies have shown that minocycline reduces infarct volume and attenuates neurological deficits in various animal models of cerebral ischemia. Preliminary clinical studies have suggested that minocycline is generally safe and well tolerated in patients with acute ischemic stroke, although evidence for its efficacy remains inconsistent. More recently, a large-scale randomized controlled trial—EMPHASIS (efficacy and safety of minocycline in patients with moderate to severe acute ischemic stroke) trial showed that short-course minocycline treatment improves 90-day functional outcomes in patients with acute ischemic stroke, without significantly increasing safety risks. Future studies should focus on identifying the target populations most likely to benefit, optimizing the therapeutic time window, dose, and treatment duration, evaluating combination strategies with reperfusion therapy, and developing novel drug-delivery approaches as well as imaging and biomarker-based evaluation systems, thereby clarifying the clinical role and translational value of minocycline in acute ischemic stroke.