Prevention and Treatment of Alzheimer's Disease by Traditional Chinese Medicine via Regulating ROS: A Review / 中国实验方剂学杂志
Chinese Journal of Experimental Traditional Medical Formulae
; (24): 281-288, 2024.
Article
em Zh
| WPRIM
| ID: wpr-1017188
Biblioteca responsável:
WPRO
ABSTRACT
The pathological mechanism of Alzheimer's disease (AD) is complex, and there are many hypotheses. The mainstream theory is the amyloid-beta protein (Aβ) and Tau protein phosphorylation. Oxidative stress (OS) is a bridge between other hypotheses and mechanisms and plays a key role in many hypotheses. Therefore, the treatment of OS in AD (ADOS) is beneficial in alleviating disease progression. Reactive oxygen species (ROS) is a kind of antioxidant and a kind of oxidation products, with Aβ and Tau protein interactions, activating microglia and astrocytes, triggering inflammation and mitochondrial dysfunction, leading to the deterioration of the environment in the brain, and accelerating the development of disease. ROS, as a signal messenger inducing OS, is widely involved in the progression of AD and may be a new target for the progression of AD. Traditional Chinese medicine (TCM) monomers and compounds play an increasingly important role in the prevention and treatment of AD. Recent studies have found that the effective prevention and treatment of AD by TCM is closely related to the regulation of ROS. There are many studies on the mechanism of TCM in the treatment of AD via regulating ROS, but there is a lack of systematic review. By analyzing and summarizing the literature in China and abroad in recent years, this paper reviewed the generation and physiology of ROS, the mechanism of action of AD, and the prevention of AD by TCM via regulating ROS through relevant ways, so as to provide references for the research on the regulation of ROS by TCM and provide new targets and new methods for the prevention and treatment of AD.
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Índice:
WPRIM
Idioma:
Zh
Revista:
Chinese Journal of Experimental Traditional Medical Formulae
Ano de publicação:
2024
Tipo de documento:
Article