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Schisandrin B protects against myocardial ischemia/reperfusion injury via the PI3K/Akt pathway in rats.

Abstract
The natural medicinal monomer, schisandrin B (Sch B), has been shown to exert cardioprotective effects; however, the underlying mechanisms of these effects remain to be fully elucidated. Therefore, the aim of the present study was to investigate whether Sch B attenuated myocardial ischemia/reperfusion (I/R) injury via the phosphoinositide 3‑kinases (PI3K)/Akt signaling pathway. To confirm this, I/R models were established in rats by ligation of the left anterior descending coronary artery. A group of animals were administered with Sch B (60 mg/kg, lavage) and/or the PI3K inhibitor, LY294002 (0.3 mg/kg, intraperitoneal). Myocardial infarct size, myocardial infarct serum markers, myocardial apoptotic index and the expression of Akt were measured in each group. The results demonstrated that the administration of Sch B reduced the size of the myocardial infarct, and this effect was eliminated following LY294002 treatment. In addition, the administration of Sch B decreased the apoptotic index and the serum markers of myocardial infarction. Sch B administration also increased the expression of phosphorylated Akt, and Sch B treatment decreased the B‑cell lymphoma 2 (Bcl‑2)‑like protein 4/Bcl‑2 ratio and the expression of cleaved caspase‑3. Therefore, Sch B may protect myocardial tissue from I/R injury via the PI3K/Akt signaling pathway in rats.
AuthorsXuyong Zhao, Yijia Xiang, Changhong Cai, Aiming Zhou, Ning Zhu, Chunlai Zeng
JournalMolecular medicine reports (Mol Med Rep) Vol. 17 Issue 1 Pg. 556-561 (Jan 2018) ISSN: 1791-3004 [Electronic] Greece
PMID29115607 (Publication Type: Journal Article)
Chemical References
  • Biomarkers
  • Cyclooctanes
  • Lignans
  • Polycyclic Compounds
  • Protective Agents
  • Troponin T
  • schizandrin B
  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt
  • Creatine Kinase, MB Form
Topics
  • Animals
  • Apoptosis
  • Biomarkers
  • Creatine Kinase, MB Form (blood)
  • Cyclooctanes (pharmacology)
  • Disease Models, Animal
  • Lignans (pharmacology)
  • Male
  • Myocardial Infarction (drug therapy, metabolism, pathology)
  • Myocardial Reperfusion Injury (drug therapy, metabolism, pathology)
  • Phosphatidylinositol 3-Kinases (metabolism)
  • Polycyclic Compounds (pharmacology)
  • Protective Agents (pharmacology)
  • Proto-Oncogene Proteins c-akt (metabolism)
  • Rats
  • Signal Transduction (drug effects)
  • Troponin T (blood)

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