Bi Shijun, Liu Shibing, Zhu Kunyuan, Gao Dandan, Chen Ligang, Yu Chunyong, Liang Guobiao
Department of Neurosurgery, General Hospital of Northern Theater Command, Shenyang, China.
Department of Neurosurgery, The Eleventh People's Hospital of Shenyang, Shenyang, China.
Front Pharmacol. 2025 Jun 27;16:1606146. doi: 10.3389/fphar.2025.1606146. eCollection 2025.
Neurological diseases such as stroke and Alzheimer's disease pose increasing challenges to global public health. Salvianolic Acid B (SalB), a major active component of , has garnered attention due to its anti-inflammatory, antioxidant, neuroprotective, and pro-angiogenic properties in neurological disease treatment.
This paper aims to review the mechanisms and effects of SalB in the treatment of neurological diseases, exploring its role in improving neurological function, mitigating neuroinflammation, and reducing oxidative stress.
SalB demonstrates multifaceted mechanisms in neurological disease management. In animal models of cerebral ischemia/reperfusion injury, SalB reduces infarct size and enhances neurological recovery via anti-inflammatory, anti-oxidative stress, and angiogenic pathways. It protects the blood-brain barrier and inhibits neuronal apoptosis in stroke models. In spinal cord injury models, SalB alleviates edema and promotes motor function recovery. In Alzheimer's disease models, SalB suppresses amyloid-beta formation and neuroinflammation. Additionally, SalB exhibits antidepressant and analgesic effects in pain-depression comorbidity models. These effects are mediated through the regulation of signaling pathways, including NF-κB, AMPK, PI3K/Akt, and Nrf2, highlighting SalB's broad therapeutic potential in neurological diseases.
SalB exhibits promising prospects in the treatment of neurological diseases. However, its clinical application faces challenges such as chemical stability and bioavailability. Further research on the mechanisms of SalB and innovative drug delivery strategies is needed to advance its application in neurological disease therapy.
中风和阿尔茨海默病等神经疾病对全球公共卫生构成了日益严峻的挑战。丹酚酸B(SalB)作为丹参的主要活性成分,因其在神经疾病治疗中的抗炎、抗氧化、神经保护和促血管生成特性而受到关注。
本文旨在综述丹酚酸B治疗神经疾病的机制和效果,探讨其在改善神经功能、减轻神经炎症和降低氧化应激方面的作用。
丹酚酸B在神经疾病管理中展现出多方面的机制。在脑缺血/再灌注损伤动物模型中,丹酚酸B通过抗炎、抗氧化应激和促血管生成途径减少梗死面积并促进神经功能恢复。它在中风模型中保护血脑屏障并抑制神经元凋亡。在脊髓损伤模型中,丹酚酸B减轻水肿并促进运动功能恢复。在阿尔茨海默病模型中,丹酚酸B抑制β-淀粉样蛋白的形成和神经炎症。此外,丹酚酸B在疼痛-抑郁共病模型中表现出抗抑郁和镇痛作用。这些作用是通过调节包括NF-κB、AMPK、PI3K/Akt和Nrf2在内的信号通路介导的,凸显了丹酚酸B在神经疾病中的广泛治疗潜力。
丹酚酸B在神经疾病治疗中展现出广阔前景。然而,其临床应用面临化学稳定性和生物利用度等挑战。需要进一步研究丹酚酸B的作用机制并创新药物递送策略,以推动其在神经疾病治疗中的应用。