Cardio-protective effects of salvianolic acid B on oxygen and glucose deprivation (OGD)-treated H9c2 cells

Artif Cells Nanomed Biotechnol. 2019 Dec;47(1):2274-2281. doi: 10.1080/21691401.2019.1621885.

Abstract

The morphological feature of apoptosis is induced by oxygen and glucose deprivation (OGD) in cardiomyocytes H9c2 cells. Salvianolic acid B (Sal-B) has been studied in several pathological progresses, whereas it is still unclear whether maternally expressed gene 3 (MEG3) is an intermediate regulator during this progress. After pre-incubation with Sal-B and stimulation with OGD, viability and apoptosis of were examined in MEG3-overexpressed H9c2 cells. Cyclin D1, apoptosis-correlated proteins and regulators of signalling pathways were quantified with Western blot assay. MEG3 was detected by quantitative reverse transcription PCR (qRT-PCR). Sal-B was implicated in the enhancement of cell viability and suppression of apoptosis in OGD-treated H9c2 cells by repressing MEG3. In addition, MEG3 overexpression exerted an inhibitory effect on murine double minute 2 (MDM2) expression while aggrandized p53 expression in OGD-treated H9c2 cells which were pre-incubated with Sal-B. Furthermore, MEG3 overexpression abolished the up-regulative effect of Sal-B on phosphorylation of adenosine monophosphate-activated protein kinase (AMPK) in OGD-treated H9c2 cells. These results indicated that cardio-protective function of Sal-B might be ascribed to its down-regulatory property on MEG3 expression which hence blocks p53 and triggers AMPK activation in OGD-treated cells.

Keywords: AMPK; MDM2/p53; MEG3; Salvianolic acid B.

MeSH terms

  • AMP-Activated Protein Kinases / metabolism
  • Animals
  • Apoptosis / drug effects
  • Benzofurans / pharmacology*
  • Cardiotonic Agents / pharmacology*
  • Carrier Proteins / metabolism
  • Cell Line
  • Down-Regulation / drug effects
  • Glucose / deficiency*
  • Mice
  • Myocytes, Cardiac / cytology
  • Myocytes, Cardiac / drug effects*
  • Myocytes, Cardiac / metabolism*
  • Oxygen / metabolism*
  • RNA, Long Noncoding / genetics
  • Signal Transduction / drug effects
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • Benzofurans
  • Cardiotonic Agents
  • Carrier Proteins
  • MEG3 non-coding RNA, mouse
  • Mtbp protein, mouse
  • RNA, Long Noncoding
  • Tumor Suppressor Protein p53
  • salvianolic acid B
  • AMP-Activated Protein Kinases
  • Glucose
  • Oxygen