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Inhibition of breviscapine on apoptosis of cultured myocardial cell of neonatal rat / 中成药
Chinese Traditional Patent Medicine ; (12)1992.
Artículo en Chino | WPRIM | ID: wpr-580418
ABSTRACT

AIM:

To investigate the inhibition of breviscapine on apoptosis of cultured myocardial cell of neonatal rat induced by hypoxia/reoxygenation.

METHODS:

Myocardial cell hypoxia/reoxygenation model was established by culturing primary myocardial cells of neonatal rats in vitro. Cultured myocardial cells were divided into 5 groupscontrol group,hypoxia/reoxygenation group and 3 groups pretreated with breviscapine of final concentration 25,50 and 100 mg/L,respectively. The cell viability was measured with MTT; apoptotic rates were determined by AnnexinV-FITC/PI; the expression of Bcl-2 was detected by immunohistochemical method. Expressions of Cytochrome C (CytC) and Caspase-3 were detected by Western blot.

RESULTS:

Compared with the control group,the viability of myocardial cell decreased and apoptosis rate elevated after hypoxia/reoxygenation. However after pretreatment with 25,50 and 100 mg/L breviscapine,respectively. Cell viabilities increased and apoptotic rates lowered,and the protective effect on myocardial cell had concentration-dependent. In addition,Expression of Bcl-2 decreased but Caspase-3 activity and CytC release increased in myocardial cells induced hypoxia/reoxygenation. Pretreated with breviscapine,expression of Bcl-2 elevated but Caspase-3 activity and CytC release reduced obviously.

CONCLUSION:

It is associated with the increase in Bcl-2 expression,inhibition of CytC release and Casepase-3 activity that breviscapine could significantly protect myocardial cell against apoptosis induced by hypoxia/reoxygenation.

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Traditional Patent Medicine Año: 1992 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Traditional Patent Medicine Año: 1992 Tipo del documento: Artículo