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Chinese Medicines Regulate p38 MAPK, ERK1/2, and JNK in Treatment of Osteoporosis: A Review / 中国实验方剂学杂志
Chinese Journal of Experimental Traditional Medical Formulae ; (24): 222-229, 2023.
Artigo em Chinês | WPRIM | ID: wpr-973152
ABSTRACT
With the aging of populationosteoporosis has become one of the main diseases endangering the health of the elderly in China. Therefore, the research on osteoporosis has become a hot spot. Since Chinese medicines demonstrate significant therapeutic effects on osteoporosis, this issue is attracting increasing attention from researchers, especially in the deciphering of the molecular mechanism. This paper introduces the mechanism of the prevention and treatment of osteoporosis by Chinese medicines via the mitogen-activated protein kinase (MAPK) signaling pathway, aiming to provide a theoretical basis for deciphering the mechanism of Chinese medicines in the treatment of osteoporosis and promoting their clinical application. MAPK signaling pathway mainly involves p38 MAPKextracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase 5 (ERK5). Studies have shown that these proteins play a role in the progression of osteoporosis by regulating cell proliferation, differentiation, and apoptosis. Chinese medicines as a unique therapy with Chinese characteristics has definite efficacy, high safety, and mild side effects. Researchers have proved by experiments that the extracts or compounds of Chinese medicines can significantly mitigate osteoporosis by regulating the proteins involved in the MAPK signaling pathway. Therefore, this article reviews the relevant studies with focus on these proteins.

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Experimental Traditional Medical Formulae Ano de publicação: 2023 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Experimental Traditional Medical Formulae Ano de publicação: 2023 Tipo de documento: Artigo