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Protection of total Flavonoids from Anchusa italica Retz, and four compounds on hypoxia-reoxygenation induced injury in myocardial cells and its mechanism / 中国药理学通报
Chinese Pharmacological Bulletin ; (12): 409-416, 2021.
Artigo em Chinês | WPRIM | ID: wpr-1014351
ABSTRACT
Aim To observe the protective effects of total flavonoids from Anchusa italica Retz, and four compounds on hypoxia/reoxygenation (H / R) injury in myocardial cells and to explore the mechanisms. Methods Primary neonatal rat cardiomyocytes were isolated, cultured and were randomly divided into different groups. The H / R model of cultured neonatal rat cardiomyocytes was developed. The related indexes were determined after administration. Results Compared with model group, the total flavonoids and the four compounds could increase the survival rate of H / R cardiomyocytes (P < 0. 01), reduce the leakage of LDH (P < 0 . 0 1), reduce the content of M DA (P < 0 . 0 1), significantly increase the activity of SOD (P <0. 01), significantly decrease the early apoptosis index and increase the mitochondrial membrane potential (P < 0. 01) . The activation of key proteins in NF-KB signaling pathway was inhibited, the proportion of Bax / Bc l - 2, beclin-1 and p62 significantly decreased (P < 0. 01), and the expression of apoptosis related proteins NLRP3, IL - lß and GSDMD significantly decreased (P <0. 0 1) . Conclusions The total flavonoids and four compounds can alleviate the damage of H/R on cardiomyocytes. The mechanism is related to the inhibition of the activation of NF-KB signaling pathway and the excessive autophagy of cardiomyocytes, alleviation of the scorch death of cardiomyocytes, and reduction of the apoptosis of cardiomyocytes.

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Pharmacological Bulletin Ano de publicação: 2021 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Pharmacological Bulletin Ano de publicação: 2021 Tipo de documento: Artigo