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Zhongguo Zhongyao Zazhi 2012-Mar

[Study on material basis of Dracocephalum moldavica for protecting cardiomyocyte against hypoxia/reoxygenation injury by traditional Chinese medicine serum chemical and pharmacological methods].

Vain rekisteröityneet käyttäjät voivat kääntää artikkeleita
Kirjaudu sisään Rekisteröidy
Linkki tallennetaan leikepöydälle
Youqing Tian
Jing Shang
Ting He
Minxuan Cai
Daoud Abdelkader

Avainsanat

Abstrakti

OBJECTIVE

To study the material basis of Dracocephalum moldavica for protecting cardiomyocyte against hypoxia/ reoxygenation injury by using traditional Chinese medicine (TCM) serum chemical and pharmacological methods.

METHODS

The extract of D. moldavica (DME) and its content absorbed into blood were determined, while blank serum and medicinal serum of rats before and after intragastrical administration of DME were also compared by HPLC. The Na2S2O4 or N2-based hypoxia/reoxygenation injury model was established by cultivating primary neonate rat cardiomyocytes or H9c2 cells in vitro. Cell viability, LDH release, T-SOD activity, MDA production and apoptosis were detected to learn the effect of DME, medicated serum and different treatments of medicinal serums under different dosage and action duration of DME on cardiomyocyte against hypoxia/reoxygenation injury.

RESULTS

Four transitional components of DME absorbed into blood after intragastrical administration were found, three of which were original components and one possible metabolite. Furthermore, compared with the model group or the blank serum group, LDH release and MDA production (P < 0.05, P < 0.01) of DME extracts, medicated serum or different treatments of medicinal serum under different dosage and action duration of DME. However, T-SOD and cell viability were improved significantly (P < 0.05, P < 0.01), while apoptosis of cardiomyocytes were also obviously inhibited.

CONCLUSIONS

The four components absorbed into blood are probably the material basis of DME used for protecting cardiomyocyte agastin hypoxia/reoxygenation injury.

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