Alpinate Oxyphyllae Fructus Inhibits IGFII-Related Signaling Pathway to Attenuate Ang II-Induced Pathological Hypertrophy in H9c2 Cardiomyoblasts

Chuan Te Tsai, Yung Ming Chang, Shu Luan Lin, Yueh Sheng Chen, Yu Lan Yeh, Viswanadha Vijaya Padma, Chin Chuan Tsai, Ray Jade Chen, Tsung Jung Ho, Chih Yang Huang

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Angiotensin II (Ang II) is a very important cardiovascular disease inducer and may cause cardiac pathological hypertrophy and remodeling. We evaluated a Chinese traditional medicine, alpinate oxyphyllae fructus (AOF), for therapeutic efficacy for treating Ang II-induced cardiac hypertrophy. AOF has been used to treat patients with various symptoms accompanying hypertension and cerebrovascular disorders in Korea. We investigated its protective effect against Ang II-induced cytoskeletal change and hypertrophy in H9c2 cells. The results showed that treating cells with Ang II resulted in pathological hypertrophy, such as increased expression of transcription factors NFAT-3/p-NFAT-3, hypertrophic response genes (atrial natriuretic peptide [ANP] and b-type natriuretic peptide [BNP]), and Gαq down-stream effectors (PLCβ3 and calcineurin). Pretreatment with AOF (60-100 μg/mL) led to significantly reduced hypertrophy. We also found that AOF pretreatment significantly suppressed the cardiac remodeling proteins, metalloproteinase (MMP9 and MMP2), and tissue plasminogen activator (tPA), induced by Ang II challenge. In conclusion, we provide evidence that AOF protects against Ang II-induced pathological hypertrophy by specifically inhibiting the insulin-like growth factor (IGF) II/IIR-related signaling pathway in H9c2 cells. AOF might be a candidate for cardiac hypertrophy and ventricular remodeling prevention in chronic cardiovascular diseases.

Original languageEnglish
Pages (from-to)300-309
Number of pages10
JournalJournal of Medicinal Food
Volume19
Issue number3
DOIs
Publication statusPublished - Mar 1 2016

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Angiotensin II
Hypertrophy
Cardiomegaly
Cardiovascular Diseases
NFATC Transcription Factors
Cerebrovascular Disorders
Natriuretic Peptides
Ventricular Remodeling
Insulin-Like Growth Factor II
Calcineurin
Matrix Metalloproteinase 2
Chinese Traditional Medicine
Matrix Metalloproteinase 9
Atrial Natriuretic Factor
Tissue Plasminogen Activator
Korea
Chronic Disease
Hypertension
Genes
Proteins

Keywords

  • alpinate oxyphyllae fructus
  • angiotensin II
  • H9c2 Cell
  • hypertrophy

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Nutrition and Dietetics

Cite this

Alpinate Oxyphyllae Fructus Inhibits IGFII-Related Signaling Pathway to Attenuate Ang II-Induced Pathological Hypertrophy in H9c2 Cardiomyoblasts. / Tsai, Chuan Te; Chang, Yung Ming; Lin, Shu Luan; Chen, Yueh Sheng; Yeh, Yu Lan; Padma, Viswanadha Vijaya; Tsai, Chin Chuan; Chen, Ray Jade; Ho, Tsung Jung; Huang, Chih Yang.

In: Journal of Medicinal Food, Vol. 19, No. 3, 01.03.2016, p. 300-309.

Research output: Contribution to journalArticle

Tsai, Chuan Te ; Chang, Yung Ming ; Lin, Shu Luan ; Chen, Yueh Sheng ; Yeh, Yu Lan ; Padma, Viswanadha Vijaya ; Tsai, Chin Chuan ; Chen, Ray Jade ; Ho, Tsung Jung ; Huang, Chih Yang. / Alpinate Oxyphyllae Fructus Inhibits IGFII-Related Signaling Pathway to Attenuate Ang II-Induced Pathological Hypertrophy in H9c2 Cardiomyoblasts. In: Journal of Medicinal Food. 2016 ; Vol. 19, No. 3. pp. 300-309.
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AU - Chang, Yung Ming

AU - Lin, Shu Luan

AU - Chen, Yueh Sheng

AU - Yeh, Yu Lan

AU - Padma, Viswanadha Vijaya

AU - Tsai, Chin Chuan

AU - Chen, Ray Jade

AU - Ho, Tsung Jung

AU - Huang, Chih Yang

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AB - Angiotensin II (Ang II) is a very important cardiovascular disease inducer and may cause cardiac pathological hypertrophy and remodeling. We evaluated a Chinese traditional medicine, alpinate oxyphyllae fructus (AOF), for therapeutic efficacy for treating Ang II-induced cardiac hypertrophy. AOF has been used to treat patients with various symptoms accompanying hypertension and cerebrovascular disorders in Korea. We investigated its protective effect against Ang II-induced cytoskeletal change and hypertrophy in H9c2 cells. The results showed that treating cells with Ang II resulted in pathological hypertrophy, such as increased expression of transcription factors NFAT-3/p-NFAT-3, hypertrophic response genes (atrial natriuretic peptide [ANP] and b-type natriuretic peptide [BNP]), and Gαq down-stream effectors (PLCβ3 and calcineurin). Pretreatment with AOF (60-100 μg/mL) led to significantly reduced hypertrophy. We also found that AOF pretreatment significantly suppressed the cardiac remodeling proteins, metalloproteinase (MMP9 and MMP2), and tissue plasminogen activator (tPA), induced by Ang II challenge. In conclusion, we provide evidence that AOF protects against Ang II-induced pathological hypertrophy by specifically inhibiting the insulin-like growth factor (IGF) II/IIR-related signaling pathway in H9c2 cells. AOF might be a candidate for cardiac hypertrophy and ventricular remodeling prevention in chronic cardiovascular diseases.

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