BNC Protects H9c2 Cardiomyoblasts from H 2 O 2 -Induced Oxidative Injury through ERK1/2 Signaling Pathway

Fangbo Zhang1, Bin Huang, Ye Zhao

  • 1Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing 100700, China.

Insights

Buchang naoxintong capsule (BNC) enhances antioxidant function and activates ERK1/2 signaling to protect H9c2 cardiomyoblasts from oxidative damage. Its cardioprotective effects against hydrogen peroxide-induced injury are comparable to trimetazidine.

Area of Science:

  • Cardiovascular medicine
  • Pharmacology
  • Cell biology

Background:

  • Buchang naoxintong capsule (BNC) is a traditional Chinese medicine for cerebrovascular and cardiovascular diseases.
  • The specific cardioprotective mechanisms of BNC against myocardial injury remain largely unknown.

Purpose of the Study:

  • To investigate the cardioprotective effects and underlying mechanisms of BNC in an in vitro model of oxidative stress.

Main Methods:

  • H9c2 rat cardiomyoblasts were subjected to hydrogen peroxide (H2O2)-induced oxidative injury.
  • BNC intestinal absorption liquid was used for preconditioning.
  • Assays included antioxidant enzyme activity, reactive oxygen species (ROS) and malondialdehyde (MDA) levels, ERK1/2 activation, apoptosis-related protein expression, intracellular Ca(2+) concentration, and mitochondrial membrane potential.

Main Results:

  • BNC preconditioning significantly enhanced antioxidant capacity (total-antioxygen, superoxide dismutase, catalase) and reduced oxidative stress markers (ROS, MDA).
  • BNC activated extracellular signal-regulated kinases (ERK1/2) and inhibited apoptosis (PARP, caspase-3).
  • BNC decreased intracellular Ca(2+) concentration, improved mitochondrial membrane potential, and reduced apoptosis rate in a dose-dependent manner.

Conclusions:

  • BNC exhibits significant cardioprotective effects against H2O2-induced oxidative injury in H9c2 cells.
  • The mechanism involves boosting antioxidant defenses, activating ERK1/2, and inhibiting Ca(2+)-dependent, mitochondria-mediated apoptosis.
  • BNC's efficacy is comparable to trimetazidine in this model.

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