Abstract
Objective
To investigate whether the administration of the ultra-filtration extract from Danggui Buxue Decoction (当归补血汤, EDBD) was able to protect cardiomyocytes from oxidative injury of rats induced by hydrogen peroxide (H2O2) and its potential mechanism.
Methods
Myocardial cells from 1- to 2-day-old neonatal rats were cultured in Dulbecco’s modified Eagle’s medium low-glucose and Ham’s F12 medium (1:1), and the cellular injury was induced by H2O2. The ultra-filtration extract mixture from Angelica sinensis and Hedysarum polybotrys was given in three doses of 3.75, 7.5, and 15 mg/mL. Morphological changes of cardiomyocytes were observed by microscope. Survival rate of myocardial cells was assessed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The cardiomyocyte damages were estimated by detecting lactate dehydrogenase (LDH) and creatine kinase (CK) releases in the medium, superoxide dismutase (SOD) activities, and intracellular malondialdehyde (MDA) and myeloperoxidase (MPO) contents. The levels of caspase-3 and heat shock protein 70 (hsp70) mRNA expression in cardiomyocytes were measured by reverse transcription polymerase chain reaction.
Results
The EDBD could protect the cardiomyocytes from H2O2 injury in a dosedependent manner (3.75, 7.50, and 15.00 mg/mL). The EDBD could significantly decrease LDH and CK leakages and intracellular MDA and MPO contents, increase SOD activity, up-regulate hsp70 expression, and down-regulate caspase-3 expression.
Conclusion
The EDBD has protection on cardiomyocytes injured by H2O2 through improving cell antioxidant ability, up-regulating hsp70 expression, and inhibiting caspase-3 activity.
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Supported by the Key Projects of the National Science and Technology Pillar Program during the Eleventh Five-Year Plan Period (No. 2007BAI37B01) and Major Science and Technology Program of Gansu Province (No. 092NKDA017)
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Li, Yd., Ma, Yh., Zhao, Jx. et al. Protection of ultra-filtration extract from Danggui Buxue Decoction (当归补血汤) on oxidative damage in cardiomyocytes of neonatal rats and its mechanism. Chin. J. Integr. Med. 17, 854–859 (2011). https://doi.org/10.1007/s11655-011-0897-6
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DOI: https://doi.org/10.1007/s11655-011-0897-6