Preclinical and experimental evidence of salvianolic acid B in the treatment of neurological diseases

丹酚酸B治疗神经系统疾病的临床前和实验证据

阅读:1

Abstract

BACKGROUND: 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 Salvia miltiorrhiza, has garnered attention due to its anti-inflammatory, antioxidant, neuroprotective, and pro-angiogenic properties in neurological disease treatment. PURPOSE: 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. RESULTS: 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. CONCLUSION: 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.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。