Syringa pinnatifolia Hemsl. fraction protects against myocardial ischemic injury by targeting the p53-mediated apoptosis pathway

Phytomedicine. 2019 Jan:52:136-146. doi: 10.1016/j.phymed.2018.09.188. Epub 2018 Sep 18.

Abstract

Background: Peeled stems of Syringa pinnatifolia Hemsl. (SP) have been widely used to treat extra "He-Yi" induced myocardial ischemia for hundreds of years in Inner Mongolia, China and previous result showed that intragastric pretreatment with total extract (T) of SP has a protective effect against myocardial infarction (MI).

Hypothesis: This study aims to describe the pharmacological investigation and chemical characterization of the major (M) and minor (N) fractions obtained from T through column chromatography fractionation on macroporous resin and to explore whether the regulatory effects were linked to the p53-mediated apoptosis pathways.

Study design: Left anterior descending (LAD) coronary artery-ligated mice and H9c2 cells cultured in serum-free medium under hypoxic conditions were treated with T, M, and N.

Methods: Echocardiography was performed and biomarkers in serum were determined in mice, and pathological changes were observed through histopathology assay. Immunofluorescence staining and qRT-PCR were used to detect the expression levels of p53 in heart tissue. Flow cytometry was used to measure the level of apoptosis and caspase-3 activity in H9c2 cells. Western blot analysis was conducted to detect p53 and p53-mediated proteins apoptosis pathways of in both tissue and H9c2 cells.

Results: Both T and M have an equivalent cardioprotective effect whereas N is non-active. M decreased MI-induced myocardial compensatory expansion by decrease of left ventricular end-systolic diameter (LVESd) and left ventricular end-diastolic diameter (LVEDd) and prevented decreases in ejection fraction (EF) and fractional shortening (FS). The MI-induced increased levels of creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), and hypersensitive C-reactive protein (hs-CRP) were decreased and the expanded infarction size was reduced. M could also improve cell viability and inhibit apoptosis in H9c2 cells under hypoxic conditions. Immunofluorescence and qRT-PCR assay showed that M suppressed p53 expression in the myocardium. Western blot analysis showed that M could prevent MI-induced activation of p53-mediated apoptosis pathway in both myocardium and H9c2 cells.

Conclusion: The results demonstrated that M may protect against myocardial ischemia by improving cardiac function and inhibiting cardiomyocytes apoptosis. Overall, the present findings supported the clinical application of SP and enriched the research of anti-myocardial ischemia drug from traditional medicines.

Keywords: Apoptosis; Hypoxia; Myocardial ischemia; Syringa pinnatifolia Hemsl.; p53; traditional medicine.

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Cardiotonic Agents / pharmacology*
  • Cell Line
  • Male
  • Mice
  • Mice, Inbred ICR
  • Myocardial Infarction / drug therapy
  • Myocardial Ischemia / drug therapy*
  • Myocardium / metabolism
  • Myocytes, Cardiac / drug effects
  • Plant Extracts / pharmacology*
  • Plant Stems / chemistry
  • Rats
  • Syringa / chemistry*
  • Tumor Suppressor Protein p53 / metabolism*

Substances

  • Cardiotonic Agents
  • Plant Extracts
  • Tumor Suppressor Protein p53