Evodiamine Inhibits Angiotensin II-Induced Rat Cardiomyocyte Hypertrophy

Na He; Qi-hai Gong; Feng Zhang; Jing-yi Zhang; Shu-xian Lin; Hua-hua Hou; Qin Wu; An-sheng Sun

doi:10.1007/s11655-017-2818-9

Your Location：

Home >

Browse articles >

Evodiamine Inhibits Angiotensin II-Induced Rat Cardiomyocyte Hypertrophy

OriginalPaper | Updated：2021-08-27

- Evodiamine Inhibits Angiotensin II-Induced Rat Cardiomyocyte Hypertrophy
- Evodiamine Inhibits Angiotensin II-Induced Rat Cardiomyocyte Hypertrophy
- 中国结合医学杂志（英文版） 2018年24卷第5期页码：359-365
- Affiliations：
  
  Key Laboratory of Basic Pharmacology of Guizhou, Department of Pharmacology, Zunyi Medical College,Guizhou Province,Zunyi,China
- Author bio：
- Funds：
  
  Supported by the National Natural Science Foundation of China (No. 81160528) and Foundation of Administration of Traditional Chinese Medicine of Guizhou Province (No. 2009-79)
- DOI：10.1007/s11655-017-2818-9
  中图分类号：
- 纸质出版日期：2018，
  
  网络出版日期：2017-9-5，
Scan for full text
He, N., Gong, Qh., Zhang, F. et al. Evodiamine Inhibits Angiotensin II-Induced Rat Cardiomyocyte Hypertrophy., Chin. J. Integr. Med. 24, 359–365 (2018). https://doi.org/10.1007/s11655-017-2818-9

Na He, Qi-hai Gong, Feng Zhang, et al. Evodiamine Inhibits Angiotensin II-Induced Rat Cardiomyocyte Hypertrophy[J]. Chinese Journal of Integrative Medicine, 2018,24(5):359-365.
He, N., Gong, Qh., Zhang, F. et al. Evodiamine Inhibits Angiotensin II-Induced Rat Cardiomyocyte Hypertrophy., Chin. J. Integr. Med. 24, 359–365 (2018). https://doi.org/10.1007/s11655-017-2818-9 DOI：

Na He, Qi-hai Gong, Feng Zhang, et al. Evodiamine Inhibits Angiotensin II-Induced Rat Cardiomyocyte Hypertrophy[J]. Chinese Journal of Integrative Medicine, 2018,24(5):359-365. DOI： 10.1007/s11655-017-2818-9.

摘要

To investigate the effects of evodiamine (Evo)

a component of Evodiaminedia rutaecarpa (Juss.) Benth

on cardiomyocyte hypertrophy induced by angiotensin II (Ang II) and further explore the potential mechanisms. Cardiomyocytes from neonatal Sprague Dawley rats were isolated and characterized

and then the cadiomyocyte cultures were randomly divided into control

model (Ang II 0.1 μmol/L)

and Evo (0.03

0.3

3 μmol/L) groups. The cardiomyocyte surface area

protein level

intracellular free calcium ([Ca2+]i) concentration

activity of nitric oxide synthase (NOS) and content of nitric oxide (NO) were measured

respectively. The mRNA expressions of atrial natriuretic factor (ANF)

calcineurin (CaN)

extracellular signal-regulated kinase-2 (ERK-2)

and endothelial nitric oxide synthase (eNOS) of cardiomyocytes were analyzed by real-time reverse transcriptionpolymerase chain reaction. The protein expressions of calcineurin catalytic subunit (CnA) and mitogen-activated protein kinase phosphatase-1 (MKP-1) were detected by Western blot analysis. Compared with the control group

Ang II induced cardiomyocytes hypertrophy

as evidenced by increased cardiomyocyte surface area

protein content

and ANF mRNA expression; increased intracellular free calcium ([Ca2+]i) concentration and expressions of CaN mRNA

CnA protein

and ERK-2 mRNA

but decreased MKP-1 protein expression (P<0.05 or P<0.01). Compared with Ang II

Evo (0.3

3 μmol/L) significantly attenuated Ang II-induced cardiomyocyte hypertrophy

decreased the [Ca2+]i concentration and expressions of CaN mRNA

CnA protein

and ERK-2 mRNA

but increased MKP-1 protein expression (P<0.05 or P<0.01). Most interestingly

Evo increased the NOS activity and NO production

and upregulated the eNOS mRNA expression (P<0.05). Evo signifificantly attenuated Ang II-induced cardiomyocyte hypertrophy

and this effect was partly due to promotion of NO production

reduction of [Ca2+]i concentration

and inhibition of CaN and ERK-2 signal transduction pathways.

Abstract

To investigate the effects of evodiamine (Evo)

a component of Evodiaminedia rutaecarpa (Juss.) Benth

on cardiomyocyte hypertrophy induced by angiotensin II (Ang II) and further explore the potential mechanisms. Cardiomyocytes from neonatal Sprague Dawley rats were isolated and characterized

and then the cadiomyocyte cultures were randomly divided into control

model (Ang II 0.1 μmol/L)

and Evo (0.03

0.3

3 μmol/L) groups. The cardiomyocyte surface area

protein level

intracellular free calcium ([Ca2+]i) concentration

activity of nitric oxide synthase (NOS) and content of nitric oxide (NO) were measured

respectively. The mRNA expressions of atrial natriuretic factor (ANF)

calcineurin (CaN)

extracellular signal-regulated kinase-2 (ERK-2)

Ang II induced cardiomyocytes hypertrophy

as evidenced by increased cardiomyocyte surface area

protein content

and ANF mRNA expression; increased intracellular free calcium ([Ca2+]i) concentration and expressions of CaN mRNA

CnA protein

and ERK-2 mRNA

but decreased MKP-1 protein expression (P<0.05 or P<0.01). Compared with Ang II

Evo (0.3

3 μmol/L) significantly attenuated Ang II-induced cardiomyocyte hypertrophy

decreased the [Ca2+]i concentration and expressions of CaN mRNA

CnA protein

and ERK-2 mRNA

but increased MKP-1 protein expression (P<0.05 or P<0.01). Most interestingly

Evo increased the NOS activity and NO production

and upregulated the eNOS mRNA expression (P<0.05). Evo signifificantly attenuated Ang II-induced cardiomyocyte hypertrophy

and this effect was partly due to promotion of NO production

reduction of [Ca2+]i concentration

and inhibition of CaN and ERK-2 signal transduction pathways.

关键词

evodiaminecardiomyocytehypertrophyangiotensin IIcalcineurinextracellular signalregulated kinase-2Nitric Oxide

Keywords

evodiaminecardiomyocytehypertrophyangiotensin IIcalcineurinextracellular signalregulated kinase-2Nitric Oxide

references

Nakaoka Y, Shioyama W, Kunimoto S, Arita Y, Higuchi K, Yamamoto K, et al. SHP2 mediates gp130-dependent cardiomyocyte hypertrophy via negative regulation of skeletal alpha-actin gene. J Mol Cell Cardiol 2010;49:157–164.

Heineke J, Molkentin JD. Regulation of cardiac hypertrophy by intracellular signalling pathways. Nat Rev Mol Cell Biol 2006;7:589–600.

Sadoshima J, Qiu Z, Morgan JP, Izumo S. Angiotensin II and other hypertrophic stimuli mediated by G protein-coupled receptors activate tyrosine kinase, mitogen-activated protein kinase, and 90-kD S6 kinase in cardiac myocytes. The critical role of Ca2+-dependent signaling. Circ Res 1995;76:1–15.

Zhao Z, Wang W, Geng J, Wang L, Su G, Zhang Y, et al. Protein kinase C epsilon-dependent extracellular signalregulated kinase 5 phosphorylation and nuclear translocation involved in cardiomyocyte hypertrophy with angiotensin II stimulation. J Cell Biochem 2010;109:653–662.

Kim S, Iwao H. Molecular and cellular mechanisms of angiotensin II-mediated cardiovascular and renal diseases. Pharmacol Rev 2000;52:11–34.

Pedram A, Razandi M, Aitkenhead M, Levin ER. Estrogen inhibits cardiomyocyte hypertrophy in vitro. Antagonism of calcineurin-related hypertrophy through induction of MCIP1. J Biol Chem 2005;280:26339–26348.

Houser, SR. Ca2+ signaling domains responsible for cardiac hypertrophy and arrhythmias. Circ Res 2009;104:413–415.

Nakayama H, Bodi I, Correll RN, Chen X, Lorenz J, Houser SR, et al. alpha1G-dependent T-type Ca2+ current antagonizes cardiac hypertrophy through α NOS3-dependent mechanism in mice. J Clin Invest 2009;119:3787–3796.

Bueno OF, Molkentin JD. Involvement of extracellular signal-regulated kinase 1/2 in cardiac hypertrophy and cell death. Circ Res 2002;91:776–781.

Marshall AK, Barrett OP, Cullingford TE, Shanmugasundram A, Sugden PH, Clerk A, et al. ERK1/2 signaling dominates over RhoA signaling in regulating early changes in RNA expression induced by endothelin-1 in neonatal rat cardiomyocytes. PLoS One 2010;5:e10027.

Fiedler B, Lohmann SM, Smolenski A, Linnemuller S, Pieske B, Schroder F, et al. Inhibition of calcineurin-NFAT hypertrophy signaling by cGMP-dependent protein kinase type I in cardiac myocytes. Proc Natl Acad Sci USA 2002;99:11363–11368.

Jiang J, Hu C. Evodiamine: a novel anti-cancer alkaloid from Evodia rutaecarpa. Molecules 2009;14:1852–1859.

Wu CL, Hung CR, Chang FY, Lin LC, Pau KY, Wang PS. Effects of evodiamine on gastrointestinal motility in male rats. Eur J Pharmacol 2002;457:169–176.

Wei J, Ching LC, Zhao JF, Shyue SK, Lee HF, Kou YR, et al. Essential role of transient receptor potential vanilloid type 1 in evodiamine-mediated protection against atherosclerosis. Acta Physiol (Oxf) 2013;207:299–307.

Bak EJ, Park HG, Kim JM, Kim JM, Yoo YJ, Cha JH. Inhibitory effect of evodiamine alone and in combination with rosiglitazone on in vitro adipocyte differentiation and in vivo obesity related to diabetes. Int J Obes (Lond) 2010;34:250–260.

Yang J, Cai X, Lu W, Hu C, Xu X, Yu Q, et al. Evodiamine inhibits STAT3 signaling by inducing phosphatase shatterproof 1 in hepatocellular carcinoma cells. Cancer Lett 2013;328:243–251.

Yu PL, Chao HL, Wang SW, Wang PS. Effects of evodiamine and rutaecarpine on the secretion of corticosterone by zona fasciculata-reticularis cells in male rats. J Cell Biochem 2009;108:469–475.

Gao YS, Sun AS, He N, Wu Q, Yang DL. Inhibitory effect of the extracts of Euodiae Fructus on right ventricular hypertrophy and calcineurin of rats. Chin Pharm (Chin) 2011;22:2508–2510.

Jiang QS, Huang XN, Yang GZ, Jiang XY, Zhou QX. Inhibitory effect of ginsenoside Rb1 on calcineurin signal pathway in cardiomyocyte hypertrophy induced by prostaglandin F2α. Acta Pharmacol Sin 2007;28:1149–1154.

Yang JH, Ma CG, Cai Y, Pan CS, Zhao J, Tang CS, et al. Effect of intermedin1-53 on angiotensin II-induced hypertrophy in neonatal rat ventricular myocytes. J Cardiovasc Pharmacol 2010;56:45–52.

Carreño JE, Apablaza F, Ocaranza MP, Jalil JE. Cardiac hypertrophy: molecular and cellular events. Rev Esp Cardiol 2006;59:473–486.

Hunter JJ, Chien KR. Signaling pathways for cardiac hypertrophy and failure. N Engl J Med 1999;341:1276–1283.

Houser, SR. Ca2+ signaling domains responsible for cardiac hypertrophy and arrhythmias. Circ Res 2009;104:413–415.

Nakayama H, Bodi I, Correll RN, Chen X, Lorenz J, Houser SR, et al. alpha1G-dependent T-type Ca2+ current antagonizes cardiac hypertrophy through a NOS3-dependent mechanism in mice. J Clin Invest 2009;119:3787–3796.

Molkentin JD. Calcineurin and beyond: cardiac hypertrophic signaling. Circ Res 2000;87:731–738.

Oka T, Dai YS, Molkentin JD. Regulation of calcineurin through transcriptional induction of the calcineurin Aß promoter in vitro and in vivo. Mol Cell Biol 2005;5:6649–6659.

Vega RB, Bassel-Duby R, Olson EN. Control of cardiac growth and function by calcineurin signaling. J Biol Chem 2003;278:36981–36984.

Bueno OF, Molkentin JD. Involvement of extracellular signal-regulated kinases 1/2 in cardiac hypertrophy and cell death. Circ Res 2002;91:776–781.

Bueno OF, De Windt LJ, Tymitz KM, Witt SA, Kimball TR, Klevitsky R, et al. The MEK1-ERK1/2 signaling pathway promotes compensated cardiac hypertrophy in transgenic mice. EMBO J 2000;19:6341–6350.

Fuller SJ, Davies EL, Gillespie-Brown J, Sun H, Tonks NK. Mitogen-activated protein kinase phosphatase 1 inhibits the stimulation of gene expression by hypertrophic agonists in cardiac myocytes. Bio chem J 1997;323:313–319.

Chu Y, Solski PA, Khosravi-Far R, Der CJ, Kelly K. The mitogen-activated protein kinase phosphatases PAC1, MKP-1, and MKP-2 have unique substrate specificities and reduced activity in vivo toward the ERK2 sevenmaker mutation. J Biol Chem 1996;271:6497–6501.

Hunter JC, Zeidan A, Javadov S, Kili A, Rajapurohitam V, Karmazyn M. Nitric oxide inhibits endothelin-1-induced neonatal cardiomyocyte hypertrophy via a RhoA-ROCKdependent pathway. J Mol Cell Cardiol 2009;47:810–818.

Saraiva RM, Hare JM. Nitric oxide signaling in the cardiovascular system: implications for heart failure. Curr Opin Cardiol 2006;21:221–228.

Janssens S, Pokreisz P, Schoonjans L, Pellens M, Vermeersch P, Tjwa M, et al. Cardiomyocyte-specific overexpression of nitric oxide synthase 3 improves left ventricular performance and reduces compensatory hypertrophy after myocardial infarction. Circ Res 2004;94:1256–1262.

Buys ES, Raher MJ, Blake SL, Neilan TG, Graveline AR, Passeri JJ, et al. Cardiomyocyte-restricted restoration of nitric oxide synthase 3 attenuates left ventricular remodeling after chronic pressure overload. Am J Physiol Heart Circ Physiol 2007;293:H620–627.

Lin Y, Liu JC, Zhang XJ, Li GW, Wang LN, Xi YH, et al. Downregulation of the ornithine decarboxylase/polyamine system inhibits angiotensin-induced hypertrophy of cardiomyocytes through the NO/cGMP-dependent protein kinase type-I pathway. Cell Physiol Biochem 2010;25:443–450.

FULL TEXT LINK

More>

浏览量

Downloads

CSCD

文章被引用时，请邮件提醒。

Submit

工具集

关联资源

Effects of serum containing Xinlikang on angiotensin II induced hypertrophy in cultured neonatal rat cardiomyocytes

Time-effect relationship of extracts from ginseng, notoginseng and chuanxiong on vascular endothelial cells senescence

Effect of Shengmai injection (生脉注射液) on diaphragmatic contractility in doxorubicin-treated rats

Metabolic regulatory and anti-oxidative effects of modified bushen huoxue decoction (补肾活血方) on experimental rabbit model of osteoarthritis