Ginkgo biloba extract reducing myocardium cells apoptosis by regulating apoptotic related proteins expression in

Zeng Yong Qiao1, Jian Hua Huang, Jiang Wei Ma

  • 1Department of Cardiology, Fengxian Branch of Shanghai 6th People's Hospital, Nanfeng road 6600#, Shanghai, 201400, China.

Molecular Biology Reports
|December 10, 2013
PubMed

Insights

Ginkgo biloba extract (GBE) reduces heart cell death and damage after ischemia/reperfusion injury in rats. GBE achieves this by down-regulating key proteins involved in apoptosis, such as Bax, cytochrome c, and caspase-3.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Pharmacology

Background:

  • Myocardial apoptosis, regulated by Bax, cytochrome c, and caspase-3, is crucial in ischemia/reperfusion (IR) injury.
  • Ginkgo biloba extract (GBE) is suspected to possess antiapoptotic properties, potentially through protein expression modulation.

Purpose of the Study:

  • To investigate the potential of GBE in attenuating IR-induced apoptosis in cardiac myocytes.
  • To elucidate the underlying mechanisms of GBE's cardioprotective effects.

Main Methods:

  • Establishment of an IR rat model.
  • Administration of GBE (400 mg/kg) to assess its effects on cardiomyocyte apoptosis and myocardial infarction.
  • Immunohistochemical and Western blot analyses to evaluate the expression levels of Bax, cytochrome c, and caspase-3 proteins.

Main Results:

  • GBE treatment significantly reduced cardiomyocyte apoptosis and myocardial infarction in the IR rat model.
  • GBE administration inhibited the IR-induced increase in myocardial Bax, caspase-3, and cytochrome c protein expression.
  • Western blot analysis corroborated the immunohistochemical findings, confirming GBE's impact on these apoptotic markers.

Conclusions:

  • GBE demonstrates a significant protective effect against myocardial IR injury in rats.
  • The cardioprotective mechanism of GBE involves the down-regulation of Bax, cytochrome c, and caspase-3 expression.
  • These findings suggest GBE's potential therapeutic role in mitigating cardiac damage associated with IR injury.

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