Xin, T., Ying, W., Jin-wen, T. et al. Effects of serum containing Xinlikang on angiotensin II induced hypertrophy in cultured neonatal rat cardiomyocytes., Chin. J. Integr. Med. 12, 194–198 (2006). https://doi.org/10.1007/BF02836521
Tu Xin, Wang Ying, Tu Jin-wen, et al. Effects of serum containing Xinlikang on angiotensin II induced hypertrophy in cultured neonatal rat cardiomyocytes[J]. Chinese Journal of Integrative Medicine, 2006,12(3):194-198.
Xin, T., Ying, W., Jin-wen, T. et al. Effects of serum containing Xinlikang on angiotensin II induced hypertrophy in cultured neonatal rat cardiomyocytes., Chin. J. Integr. Med. 12, 194–198 (2006). https://doi.org/10.1007/BF02836521DOI:
Tu Xin, Wang Ying, Tu Jin-wen, et al. Effects of serum containing Xinlikang on angiotensin II induced hypertrophy in cultured neonatal rat cardiomyocytes[J]. Chinese Journal of Integrative Medicine, 2006,12(3):194-198. DOI: 10.1007/BF02836521.
Effects of serum containing Xinlikang on angiotensin II induced hypertrophy in cultured neonatal rat cardiomyocytes
摘要
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 α-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 μg/L in the model group
and 430 ±23 ώg/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 i 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).Conclusion: 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.
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 α-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 μg/L in the model group
and 430 ±23 ώg/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 i 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).Conclusion: 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.
关键词
Xinlikangangiotensin IIcardiomyocytehypertrophy
Keywords
Xinlikangangiotensin IIcardiomyocytehypertrophy
references
Flack JM, Peters R, Shafi T, et al. Prevention of hypertension and its complications: theoretical basis and guidelines for treatment. J Am Soc Nephrol 2003;14 (7 Suppl 2): S92-S98.
Arima S. Role of angiotensin II and endogenous vasodilators in the control of glomerular hemodynamics. Clin Exp Nephrol 2003;7: 172–178.
Tu X, Wang JM, Tu Q, et al. Effects of peucedanum praeruptorum dunn extract on left ventricular remodeling and Bcl-2, Bax protein expression in aorta coarctation rats. Chin J Clin Pharmacol Ther 2004;9(4): 394–397.
Tarnavski O, McMullen JR, Schinke M, et al. Mouse cardiac surgery: comprehensive techniques for the generation of mouse models of human diseases and their application for genomic studies. Physiol Genomics 2004;16: 349–360.
Delyani JA, Rocha R, Cook CS, et al. Eplerenone: a selective aldosterone receptor antagonist (SARA). Cardiovasc Drug Rev 2001;19: 185–200.
DeMello WC, Danser AH. Angiotensin II and the heart: on the intracrine renin-angiotensin system. Hypertension 2000;35: 1183–1188.
Ishii K, Takekoshi K, Shibuya S, et al. Angiotensin subtype-2 receptor (AT2) negatively regulates subtype-1 receptor (ATI) in signal transduction pathways in cultured porcine adrenal medullary chromaffin cells. J Hypertens 2001;19: 1991–1999.
Matsubara H. Renin-angiotensin system in human failing hearts message from nonmyocyte cells to myocytes. Circ Res 2001;88: 861–863.
Kawano H, Do YS, Kawano Y, et al. Angiotensin II has multiple profibrotic effects in human cardiac fibroblasts. Circulation 2000: 101: 1130–1137.
Castoldi G, diGioia CR, Pieruzzi F, et al. ANG II increases TIMP-1 expression in rat aortic smooth muscle cellsin vivo. Am J Physiol Heart Circ Physiol 2003; 284: 635–643.
Chien KR, Grace AA, Hunter JJ. Molecular basis of cardiac hypertrophy and heart failure. In Chein KR (ed): Molecular Basis of Heart Disease. Philadelphia, W. B. Saunders Company, 1997: 193.
Morgan HE, Baker KM. Cardiac hypertrophy: Mechanical, neural and endocrine dependence. Circulation 1991; 83: 13–25.
Katz AM. Scientific insights from clinical studies of converting-enzyme inhibitors in failing heart. Trends Cardiovasc Med 1995;5(1): 37–44.