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Regulatory mechanism of p38MAPK signaling pathway on renal tissue inflammation in chronic kidney disease and interventional effect of traditional Chinese medicine / 中国中药杂志
China Journal of Chinese Materia Medica ; (24): 1700-1704, 2012.
Artículo en Chino | WPRIM | ID: wpr-338778
ABSTRACT
The inflammatory reaction of renal tissues and its relevant tissue damages (such as glomerulosclerosis and renal interstitial fibrosis) are important factors for the development of chronic kidney diseases (CKD) to end-state renal diseases. Of them, p38 mitogen-activated protein kinase (MAPK) signaling pathway plays an important role in regulating expression and bioactivity of multiple nuclear transcription factors, impacting synthesis of downstream inflammatory mediators and activating inflammatory cells. Some monomer traditional Chinese medicines and their extracts (such as emodin and berberine) and some traditional Chinese medicine compound prescriptions (such as Yishen Huoxue decoction) can affect inflammatory reaction of renal tissues by regulating p38MAPK signaling pathway, thas improving reduce glomerulus and renal interstitial inflammatory injury.
Asunto(s)
Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Patología / Transducción de Señal / Enfermedad Crónica / Proteínas Quinasas p38 Activadas por Mitógenos / Quimioterapia / Inflamación / Enfermedades Renales / Medicina Tradicional China / Metabolismo / Métodos Tipo de estudio: Estudio diagnóstico Límite: Animales / Humanos Idioma: Chino Revista: China Journal of Chinese Materia Medica Año: 2012 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Patología / Transducción de Señal / Enfermedad Crónica / Proteínas Quinasas p38 Activadas por Mitógenos / Quimioterapia / Inflamación / Enfermedades Renales / Medicina Tradicional China / Metabolismo / Métodos Tipo de estudio: Estudio diagnóstico Límite: Animales / Humanos Idioma: Chino Revista: China Journal of Chinese Materia Medica Año: 2012 Tipo del documento: Artículo