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

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Evodiamine Inhibits Angiotensin II-Induced Rat Cardiomyocyte Hypertrophy

Updated：2021-08-27

- Evodiamine Inhibits Angiotensin II-Induced Rat Cardiomyocyte Hypertrophy
- Chinese Journal of Integrative Medicine Vol. 24, Issue 5, Pages: 359-365(2018)
- 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
  CLC：
- Published：2018，
  
  Published Online：5 September 2017，
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 24(5):359-365(2018)
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 24(5):359-365(2018) 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

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