title: Cardioprotective effects of fucoidan against hypoxia-induced apoptosis in H9c2 cardiomyoblast cells.
abstract: BACKGROUND
  Cardiomyocyte apoptosis plays a critical role in the progress of heart diseases. Fucoidan, a complex-sulfated polysaccharide, has been reported to possess potential cardioprotective efficacy in vivo.
  
  
  OBJECTIVE
  The present study determines whether fucoidan could provide cardioprotection on hypoxia-induced cardiomyocyte apoptosis.
  
  
  METHODS
  H9c2 cardiomyoblast cells were incubated with various concentrations (15, 30, and 60 μg/ml) of fucoidan in a humidified incubator at 37 °C with 95% O2 and 5% CO2. After 6 h, hypoxia was processed and the cardioprotective effects of fucoidan were evaluated by applying MTT, ELISA, Hoechst 33258 nucleus staining, and western blot.
  
  
  RESULTS
  Following a 6 h exposure of H9c2 to hypoxic condition, significant reduction was found in cell survival (0.57-fold) and superoxide dismutase (SOD) activity (0.56-fold), which were associated with the increase of malondialdehyde (MDA) level (2.58-fold), creatine phosphokinase (CK, 3.57-fold), and lactate dehydrogenase (LDH) activities (2.39-fold). Moreover, hypoxia-induced apoptosis was confirmed by Hoechst 33258 nuclear staining, and these changes were accompanied by the increase of Bcl-2 (1.27-fold) and Bax expression (2.6-fold). However, preincubation of the cells with fucoidan prior to hypoxia exposure elevated the cell viability (30 μg/ml, 1.18-fold; 60 μg/ml, 1.32-fold) and SOD activity (30 μg/ml, 1.12-fold; 60 μg/ml, 1.25-fold), but decreased the MDA level (30 μg/ml, 0.70-fold; 60 μg/ml, 0.80-fold), CK (30 μg/ml, 0.69-fold; 60 μg/ml, 0.76-fold), and LDH (30 μg/ml, 0.67-fold; 60 μg/ml, 0.86-fold) leakages. Hoechst 33258 nuclear staining observations demonstrated the same protective effect of fucoidan on hypoxia-induced myocardial injury. Also, cardioprotective effects of fucoidan were reflected by increasing Bcl-2 (60 μg/ml, 1.84-fold), as well as decreasing Bax (60 μg/ml, 0.6-fold).
  
  
  CONCLUSIONS
  Fucoidan had protective effect against hypoxia-induced cardiomyocytes apoptosis, and the mechanism might involve protections of the cell from oxidative injury.
authors: School of Pharmacy, Binzhou Medical College , Yantai , China and.
authors: S M
authors: SM
authors: Zhang
authors: Z P
authors: ZP
authors: Xie
authors: M L
authors: ML
authors: Xu
authors: L F
authors: LF
authors: Shi
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D015415:Biomarkers / Q000378:metabolism; D015687:Cell Hypoxia; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D003402:Creatine Kinase / Q000378:metabolism; D019610:Cytoprotection; D004305:Dose-Response Relationship, Drug; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D032386:Myoblasts, Cardiac / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D011134:Polysaccharides / Q000494:pharmacology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D013482:Superoxide Dismutase / Q000378:metabolism; D013997:Time Factors; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D000975:Antioxidants; C494828:Bax protein, rat; D015415:Biomarkers; D011134:Polysaccharides; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D008315:Malondialdehyde; C007789:fucoidan; D007770:L-Lactate Dehydrogenase; D013482:Superoxide Dismutase; D003402:Creatine Kinase
keywords: Amelioration; cardiac enzymes; cell toxicity; in vitro test; sulfated polysaccharide