
FOLLOWUS
1. 1Department of Community Health Nursing, Liaoning Medical University, Jinzhou, Liaoning 121001, China
2Department of Biochemistry and Molecular Biology, Liaoning Medical University, Jinzhou, Liaoning 121001, China
3. 3Centre of Scientific Experiment, Liaoning Medical University, Jinzhou, Liaoning 121001, China
*Corresponding author Tel: 86-416-4605084, E-mail: jy2006hldai@sohu.com, jiaguizhi2006@163.com
收稿日期:2014-07-25,
网络出版日期:2015-02-20,
纸质出版日期:2015-02
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Total Glycosides of
Dai Hong-liang, Jia Gui-zhi, Zhao Song. Total Glycosides of
Total Glycosides of
Dai Hong-liang, Jia Gui-zhi, Zhao Song. Total Glycosides of
Objective
To evaluate the
in vitro
anti-hypertrophic effect of total Glycosides of
Ranunculus Japonius
(TGRJ).
Methods
Neonatal rat cardiomyocytes were cultured and hypertrophy was induced by adminis- trating isoproterenol (ISO
10 µmol/L) or angiotensin Ⅱ (Ang Ⅱ
1 µmol/L) for 48 hours. In the treatment groups
cells were pretreated with TGRJ (0.3 g/L) for 30 minutes prior to hypertrophic stimuli. The anti-hypertrophic effects of TGRJ were examined by measuring cell size
total protein content
and protein synthesis. Intracellular free Ca
2+
concentration ([Ca
2+
]
i
) was evaluated using fluorescence dye Fura-2/AM. Sacroplasmic/endoplasmic reticulum Ca
2+
ATPase 2a (SERCA2a)
atrial natriuretic peptide (ANP)
B-type natriuretic peptide (BNP)
and beta-myosin heavy chain (β-MHC) protein expression levels were measured by Western blotting . SERCA2a activity was assayed by p-nitrophenal phosphate disodium salt hexahydrate method.
Results
Increased cell size
total protein content
and protein synthesis following ISO or Ang Ⅱ stimulation were significantly inhibited by pretreatment with TGRJ (all
P
<
0.05). This anti-hypertrophic effect of TGRJ was confirmed by its suppressing effect on elevated expression of the three hypertrophic related genetic markers
ANP
BNP
and β-MHC. In addition
TGRJ inhibited ISO or Ang Ⅱ induced up-regulation of [Ca
2+
]
i
under chronic but not acute conditions. And ISO or Ang Ⅱ induced down-regulation of SERCA2a expression and activity was also effectively rectified by TGRJ pretreatment.
Conclusions
The results of present study suggested that TGRJ could prevent ISO or Ang Ⅱ induced cardiac hypertrophy through improving chronic [Ca
2+
]
i
disorder
might
via
normalizing SERCA2a expression and activity.
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