Zhou Z.-H.,Key Laboratory of Molecular Biology and New Drug Research |
Wang H.-X.,Key Laboratory of Molecular Biology and New Drug Research |
Zhao S.-L.,Key Laboratory of Molecular Biology and New Drug Research |
Yu X.-C.,Chinese Academy of Sciences |
And 2 more authors.
Chinese Traditional and Herbal Drugs | Year: 2012
Objective To investigate the protective effect of astragalus polysaccharide (APS) on lipopolysaccharide (LPS)-induced cardiac myocytes hypertrophy of rats and its mechanism. Methods Cardiac myocytes of 1-2 d neonatal SD rats were cultured 48 h in vitro, and divided into control, model (LPS 1 mg/L) group, APS low-, middle-, and high- (1, 10, and 100 mg/L) groups. The cardiomyocyte volume was assayed by computer photograph analysis; atrial natriuretic peptide (ANP) mRNA expression was measured by RT-PCR; and tumor necrosis factor-α (TNF-α) level was determined by ELISA. The transient peak change of intracellular calcium concentration ([Ca 2+] i) was measured by using Fluo-3/Am fluorescent dye load cell under laser confocal microscope. Results Compared with control group, LPS 1 mg/L could make the volume of myocardial cells, ANP mRNA expression, the release of TNF-α protein, and [Ca 2+] i transient peak increase significantly (P < 0.01). Compared with the LPS model group, APS pre-administrated at the concentrations of 1, 10, and 100 mg/L could inhibit myocardial cell volume increase, while cells of TNF-α were significantly reduced, ANP mRNA expression decreased in varying degrees (P < 0.05). APS 10 and 100 mg/L groups could be restored to normal levels of the control group (P > 0.05) and APS 10 mg/L could antagonize transient changes in amplitude increase of [Ca 2+] i in normal cardiac myocytes (P < 0.01). Conclusion APS does have a good protection on cultured cardiac myocytes hypertrophy and its mechanism may be related to the inhibition of [Ca 2+] i. Source