Safflor Yellow A Protects Neonatal Rat Cardiomyocytes Against Anoxia/reoxygenation Injury in Vitro

Overview

Journal Acta Pharmacol Sin

Specialty Pharmacology

Date 2013 Feb 12

PMID 23396376

Citations 18

Authors

Jia-Lin Duan

Jing-Wen Wang

Yue Guan

Ying Yin

Guo Wei

Jia Cui

Dan Zhou

Yan-Rong Zhu

Wei Quan

Miao-Miao Xi

Ai-Dong Wen

Affiliations

Soon will be listed here.

Abstract

Aim: To investigate the effects of safflor yellow A (SYA), a flavonoid extracted from Carthamus tinctorius L, on cultured rat cardiomyocytes exposed to anoxia/reoxygenation (A/R).

Methods: Primary cultured neonatal rat cardiomyocytes were exposed to anoxia for 3 h followed by reoxygenation for 6 h. The cell viability was measured using MTT assay. The releases of lactate dehydrogenase (LDH) and creatine kinase (CK), level of malondialdehyde (MDA), and activities of glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were analyzed. Hoechst 33258 staining and changes in Bcl-2/Bax ratio and caspase 3 activity were used to examine A/R-induced apoptosis.

Results: The A/R exposure markedly decreased the viability of cardiomyocytes, suppressed the activities of SOD, GSH, CAT and GSH-Px, and Bcl-2 protein expression. Meanwhile, the A/R exposure markedly increased the release of LDH and CK, and MDA production in the cardiomyocytes, and increased the rate of apoptosis, caspase 3 activity, Bax protein expression. Pretreatment with SYA (40, 60 and 80 nmol/L) concentration-dependently blocked the A/R-induced changes in the cardiomyocytes. Pretreatment of the cardiomyocytes with the antioxidant N-acetylcysteine (NAC, 200 μmol/L) produced protective effects that were comparable to those caused by SYA (80 nmol/L).

Conclusion: SYA protects cultured rat cardiomyocytes against A/R injury, maybe via inhibiting cellular oxidative stress and apoptosis.

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