title: Effects of serum containing Xinlikang on angiotensin ii induced hypertrophy in cultured neonatal rat cardiomyocytes.
abstract: OBJECTIVE
  To evaluate the effects of Xinlikang (XLK) on angiotensin II (Ang II) induced hypertrophic cultured neonatal rat's cardiomyocyte (CMC).
  
  
  METHODS
  Primary cultured neonatal rat's CMCs with the purity certified by immunohistochemical technique, were divided into three groups. Rats in the normal control group were untreated; those in the model group were established into hypertrophic models but underwent no treatment; and those in the XLK group were established to hypertrophic models and treated with XLK containing serum obtained from rats with aorta coarctation after 8 days of feeding with XLK. MTT and phase-contrast microscope were used to evaluate the effect of XLK on cell activity, pulsating rhythm and surface area; Atrial natriuretic peptide (ANP) expression was determined by radioimmunoassay; Protein content was determined by Bradford method; and DNA synthesis was detected by flow cytometric assay.
  
  
  RESULTS
  Immunohistochemistry results showed that more than 90% of the cells were alpha-sarcometin actin stained positive cells. No significant effect of XLK on normal CMC was found. Ang II could significantly induce hypertrophy in CMCs, and XLK could significantly decrease the increased surface area and the accelerated pulsating rate in them. ANP expression was 780 +/- 38 microg/L in the model group, and 430 +/- 23 microg/L in the control group, and the elevated expression of ANP in model rats was significantly decreased in the XLK group; The DNA content in the G0/G1 and G2/M phases was significantly enhanced and at the same time it was accompanied with increase of total protein content in the model rats after being stimulated by Ang II for 24 h, showing that serum-containing XLK could also significantly suppress total protein synthesis (P < 0.05).
  
  
  CONCLUSIONS
  XLK could improve Ang II mediated pathological growth of CMCs without influencing the growth of normal CMCs, suggesting that XLK is probably an effective drug for treatment of myocardial hypertrophy and heart failure.
authors.affiliation: Center for Human Genome Research, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China. partner@public.wh.hb.cn
authors.forename: Xin
authors.initials: X
authors.lastname: Tu
authors.forename: Ying
authors.initials: Y
authors.lastname: Wang
authors.forename: Jin-wen
authors.initials: JW
authors.lastname: Tu
authors.forename: Yi
authors.initials: Y
authors.lastname: Yang
authors.forename: Jin-ming
authors.initials: JM
authors.lastname: Wang
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D000831:Animals, Newborn; D009320:Atrial Natriuretic Factor / Q000378:metabolism; D048429:Cell Size / Q000187:drug effects; D002478:Cells, Cultured; D004247:DNA / Q000096:biosynthesis; D004365:Drugs, Chinese Herbal / Q000494:pharmacology*; D006984:Hypertrophy; D009200:Myocardial Contraction / Q000187:drug effects; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology*; D011506:Proteins / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D014662:Vasoconstrictor Agents / Q000494:pharmacology*
chemical_list: D004365:Drugs, Chinese Herbal; D011506:Proteins; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D009320:Atrial Natriuretic Factor; D004247:DNA