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Protective effect of tanshinone II A on signal
transduction system protein kinase B in rats with myocardial hypertrophy |
Enyuan TU MD,Yongjun PAN MM,Kang ZHENG MM,Zhaohua WANG MD,Qiansheng LIANG MD,Guangtian YANG MD, |
Department of Emergency,
Tongji Hospital, Tongji Medical College, Huazhong University of Science
and Technology, Wuhan 430030, China; |
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Abstract The effects of tanshinone II A on cell signal transduction system protein kinase B in rats with myocardial hypertrophy induced by the abdominal aorta partial coarctation were investigated. Rat models of myocardial hypertrophy were established by using abdominal aorta partial coarctation method. Forty-eight rats were randomly divided into sham group (S group), model group (M group), valsartan treatment group (X group), low-dose tanshinone treatment group (LD group), medium-dose tanshinone treatment group (MD group), and high-dose tanshinone treatment group (HD group) (n=8 in each group). Left ventricular mass index (LVMI), left ventricular posterior wall (LVPW), and septal thickness (IVS) were detected by high frequency ultrasonography. Myocardial fiber diameter (MFD) was examined by Hematoxylin-Eosin (HE) staining, and the contents of phosphorylated protein kinase B (p-Akt) and p-Gsk3β in myocardium were assayed by Western blot. The results showed that compared with S group, the values of LVMI, LVPW, IVS and MFD were increased in other groups (P<0.05), and the contents of p-Akt, and p-Gsk3β were also increased in other groups. As compared with MD group, the values of LVMI, LVPW, IVS and MFD were decreased in all treatment groups (P<0.05), and the contents of p-Akt, and p-Gsk3β were also decreased in all treatment groups. However, there were no significant differences among LD, MD, and HD groups (P>0.05), and there were no significant differences between X group and tanshinone treatment groups (P>0.05). It was suggested that tanshinone II A could prevent myocardial hypertrophy by its action on the Akt signaling pathway.
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Keywords
tanshinone II A
myocardial hypertrophy
rat
protein kinase B
abdominal aorta coarctation
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Issue Date: 05 December 2009
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Kang Y J. Cardiac hypertrophy: a risk factor for QT2prolon2 gation and cardiacsudden death. Toxicol Pathol, 2006, 34(10): 58–66
doi: 10.1080/01926230500419421
|
|
Sun L P, Zheng Z. The effects of sodium tanshinoneII A sulfonate on activation of NF-κB on hypertrophic myocardialcells. Shiyong Laonian Yixue, 2004, 18(1): 25–27 (in Chinese)
|
|
Xu S Y, Bian R L, Chen X. Pharmacological experiments methodology. Beijing: People’ HealthPress, 2002, 1026–1028
|
|
Frey N, Olson E N. Cardiac hypertrophy: thegood, the bad, and the ugly. Ann Rev Physiol, 2003, 65: 45–79
doi: 10.1146/annurev.physiol.65.092101.142243
|
|
James M A, Saadeh A M, Jones J V. Wall stress and hypertension. J Cardiovasc Risk, 2000, 30(7): 187–190
|
|
Spirito P, Autore C. Management of hypertrophiccardiomyopathy. BMJ, 2006, 322(7552): 1251–1255
doi: 10.1136/bmj.332.7552.1251
|
|
Hu J, Zhang C T, Pu J, Quan X Q, Lv J G, Bai R, Wei Y, Zeng X L. Effects of Perindopril on Ventricular Arrhythmias inRabbits with Cardiac Hypertrophy. Hua ZhongKe Ji Da Xue Xue Bao (Yi Xue Ban), 2008, 37(5): 688–690 (in Chinese)
|
|
Ke J, Zhang C T, Ma Y X, Liu J, Liu N, Ruan Y F, Lin L. The Roles of Calmodulin KinaseII Inhibitor in Ventricular Arrhythmias in Rabbits with Cardiac Hypertrophy. Hua Zhong Ke Ji Da Xue Xue Bao (Yi Xue Ban), 2007, 36(2): 183–190 (in Chinese)
|
|
Li L F, Chen L W. The mechanisms of myocardialhypertrophy. Hai Nan Yi Xue, 2008, 19(7): 123–125 (in Chinese)
|
|
Wang Y. Signaltransduction in cardiac hypertrophy-dissecting compensatory versuspathological pathways utilizing a transgenic approach. Curr Opin Pharmacol, 2001, 41(1): 134–140
doi: 10.1016/S1471-4892(01)00029-7
|
|
Morisco C, Zebroski D, Condorelli G. The Akt-glycogen synthase kinase 3β pathway regulatestranscription atrial natriiuretic factor induced by β-adrenergicreceptor stimulation in cardiac myocytes. J Biol Chem, 2000, 275(19): 14466–14475
doi: 10.1074/jbc.275.19.14466
|
|
Matsui T, Nagoshi T, Rosenzweig A. Akt and PI 3-kinase signaling in cardiomyocyte hypertrophyand survival. Cell Cycle, 2003, 2(3): 220–223
|
|
Cao W, Shi F X, Phosphodiesterase type 3B:Downstream Factor of PI3k/PKB pathway as well as its clinical research, Xi Bao Sheng Wu Xue Za Zhi, 2007, 29(6): 800–804 (in Chinese)
|
|
Frame S, Cohen P. GSK3 takes centre stage morethan 20 years after its discovery. BiochemJ, 2001, 359(1): 1–16
doi: 10.1042/0264-6021:3590001
|
|
Antos C L, McKinsey T A, Frey N, Kutschke W, McAnally J, Shelton J M, Richardson J A, Hill J A, Olson E N. Activated glycogen synthase-3β suppresses cardialhypertrophy in vivo. Proc Natl Acad SciUSA, 2002, 99(2): 907–912
doi: 10.1073/pnas.231619298
|
|
Shio Jima I, Walsh K. Regulation of cardiac growthand coronary angiogenesis by the Akt/PKB signaling pathway. Genes Dev, 2006, 20(24): 3347–3365
doi: 10.1101/gad.1492806
|
|
Heineke J, Molkentin J D. Regulation of cardiac hypertrophyby intracellular signaling pathways. NatRev Mol Cell Biol, 2006, 7(8): 589–600
doi: 10.1038/nrm1983
|
|
Balakumar P, Singh M. The possible role of caspase-3in pathological and physiological cardiac hypertrophy in rats. Basic Clin Pharmacol Toxicol, 2006, 99(6): 418–424
doi: 10.1111/j.1742-7843.2006.pto_569.x
|
|
Gao N, Flynn D C, Zhang Z. G1 cell cycle progression and the expression of G1 cyclinsare regulated by PI3K/AKT/mTOR/p70S6K1 signaling in human ovariancancer cells. Am J Physiol Cell Physiol, 2004, 287(2): C281–C291
doi: 10.1152/ajpcell.00422.2003
|
|
Matsui T, Li L, Wu J C, Cook S A, Naqoshi T, Picard M H, Liao R, Rosenzweiq A. Phenotypix spectrum caused by transgenic overexpressionof activated Akt in the heart. J Biol Chem, 2002, 277(25): 22896–22901
doi: 10.1074/jbc.M200347200
|
|
Shioi T, Mcmullen J R, Kang P M, Douqlas P S, Obata T, Franke T F, Cantley L C, Izumo S. Akt/Protein kinase B promotesorgan growth in transgenic mice. Mol CellBiol, 2002, 22(8): 2799–2809
doi: 10.1128/MCB.22.8.2799-2809.2002
|
|
McMullen J R, Izumo S. Role of the insulin-likegrowth factor 1 (IGF1)/phosphoinositide-3-kinase (PI3K) pathway mediatingphysiological cardiac hypertrophy. NovartisFound Symp, 2006, 274: 90–111
doi: 10.1002/0470029331.ch7
|
|
Zhou Y, Zhang J P, Wu M H, Liu H, Zhao Z G, He S Y, Wang Y T, Chu L. Influence of “YiQi QiangXin Decoction” onpressure overload myocardial hypertrophy. Shang Hai Zhong Yi Yao Za Zhi, 2008, 42(5): 80–82 (in Chinese)
|
|
Sun L P, Zheng Z. The Effect of Salvia MiltiorrhizaBge on left ventricular hypertrophy and the expression of tumor necrosisfactor-α in spontaneously hypertensive rats. Gao Xue Ya Za Zhi, 2004, 12(3): 238–241 (in Chinese)
|
|
Gong L Y, Zheng Z, Xiong W, Sun L P. TanshinoneⅡAprevents angiotensinⅡ-induced hypertrophy of cardiomyocytes from rat. Hua Xi Yao Xue Za Zhi, 2004, 9(1): 24–27 (in Chinese)
|
|
Jiang F L, Feng J, Zheng Z. Effect of sodium tanshinone II-Asulfonate on activation of extracellular signal-regulated kinase 1/2in angiotensin II-induced cardiomyocyte hypertrophy. Zhong Guo Yao Li Xue Tong Bao, 2008, 24(3): 307–312 (in Chinese)
|
|
Li Y S, Wang Z H, Wang J, Yan L, Yong Y Q, Liang Q S, Zheng Z, Yang G T. Effect of tashinone ⅡA on the nitric oxide synthase geneexpression and intracellular Ca~(2+) level in the hypertrophic cadiocytesof pressure-overloaded rats. Hua ZhongKe Ji Da Xue Xue Bao (Yi Xue Ban), 2008, 37(3): 286–289 (in Chinese)
|
|
Yang T, Zhang W, Zhang L. Inhibitory effects of L-arginine-nitric oxide pathwayon formation of pathological cardiac hypertrophy and the related mechanisms. Di Er Jun Yi Da Xue Xue Bao, 2008, 29(2): 177–183 (in Chinese)
|
|
Ouyang X, Takahashi K, Komatsu K, Nakamura N, Hattori M, Baba A, Azuma J. Protectiveeffect of salvia miltiorrhiza on angiotensin Ⅱ induced hypertrophicresponses in neonatal rat cardial cells. Jpn J pharmacol, 2001, 87(4): 289–296
doi: 10.1254/jjp.87.289
|
|
Pan G J, Wang X L. Effect of Radix Salviae Miltiorrhizae(RAM) on myocardiac hypertrophy in rat model of over-loading pressure. Zhong Guo Fen Zi Xin Zhang Bing Xue Za Zhi, 2007, 7(1): 34–36 (in Chinese)
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