Nardosinone protects H9c2 cardiac cells from angiotensin II-induced hypertrophy

Du, Meng; Huang, Kun; Liu, Yang; Wang, Wen Shuo; Wang, Bo; Huang, Kai; Huang, Dan

doi:10.1007/s11596-013-1205-9

Cited by 19 publications

(13 citation statements)

References 21 publications

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“…It was found that, in murine MI/R injury models, the mRNA level of Ang II markedly increased in hearts on day 28, but VCP979 treatment reversed this elevation. consistent with previous reports (41,46), the addition of Ang II induced significant collagen synthesis in NcFs and hypertrophy in NcMs. The present results further revealed that the addition of VcP979 prevented NcFs from Ang II-induced collagen synthesis and NcMs from Ang II-induced hypertrophy in the cell culture system.…”

Section: Discussionsupporting

confidence: 93%

A novel small molecule compound VCP979 improves ventricular remodeling in murine models of myocardial ischemia/reperfusion injury

Liu

Meng²,

Liang³

et al. 2019

Int J Mol Med

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Persistent ventricular remodeling following myocardial ischemia/reperfusion (MI/R) injury results in functional decompensation and eventual progression to heart failure. VcP979, a novel small-molecule compound developed in-house, possesses anti-inflammatory and anti-fibrotic activities. In the present study, no significant pathological effect was observed following the administration of VCP979 on multiple organs in mice and no difference of aspartate transaminase/alanine aminotransferase/lactate dehydrogenase levels was found in murine serum. Treatment with VcP979 ameliorated cardiac dysfunction, pathological myocardial fibrosis and hypertrophy in murine MI/R injury models. The administration of VCP979 also inhibited the infiltration of inflammatory cells and the pro-inflammatory cytokine expression in hearts post MI/R injury. Further results revealed that the addition of VcP979 prevented the primary neonatal cardiac fibroblasts (NCFs) from Angiotensin II (Ang II)-induced collagen synthesis and neonatal cardiac myocytes (NcMs) hypertrophy. In addition, VcP979 attenuated the activation of p38-mitogen-activated protein kinase in both Ang II-induced NCFs and hearts subjected to MI/R injury. These findings indicated that the novel small-molecule compound VcP979 can improve ventricular remodeling in murine hearts against MI/R injury, suggesting its potential therapeutic function in patients subjected to MI/R injury.

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Section: Discussionsupporting

confidence: 93%

A novel small molecule compound VCP979 improves ventricular remodeling in murine models of myocardial ischemia/reperfusion injury

Liu

Meng²,

Liang³

et al. 2019

Int J Mol Med

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“…The hypertrophic response of H9c2 cells was induced by angiotensin II (1µmol/L) incubating for 24h [20]. Neonatal rats’ ventricular myocytes (NRVM) from 1-2 days old Sprague-Dawley rats were cultured as described previously [21, 22].…”

Section: Methodsmentioning

confidence: 99%

Cyclin-Dependent Kinase Inhibitor p21WAF1/CIP1 Facilitates the Development of Cardiac Hypertrophy

Tong

Wang

Ding

et al. 2017

Cell Physiol Biochem

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Background/Aims: Adult cardiomyocytes can re-enter cell cycle as stimulated by prohypertrophic factors although they withdraw from cell cycle soon after birth. p21^WAF1/CIP1, a cyclin-dependent kinase inhibitor, has been implicated in cardiac hypertrophy, however, its precise contribution to this process remains largely unclear. Methods: The gene expression profile in left ventricle (LV) of spontaneously hypertensive rats (SHR) and Wistar–Kyoto (WKY) rats was determined using quantitative PCR array and verified by real-time PCR and Western blotting. Hypertrophic response of H9c2 cells and neonatal rat ventricular myocytes (NRVM) were induced by angiotensin II (1 µmol/L). Cardiac hypertrophy of mice was elicited by isoproterenol (ISO) infusion (40 mg/kg per day for 14 days). p21-adenovirus and p21-siRNA were employed to transfect NRVM, and sterigmatocystin (STE, 3 mg/kg, ip, qd) was used to inhibit p21 activity. mRNA and protein expression levels of α- and β-myosin heavy chain (MHC), p21^WAF1/CIP1, calcineurin (CaN) and atrial natriuretic peptide (ANP) were assayed by realtime PCR and WB, respectively. Results: Sixteen genes showed two-fold or greater changes between SHR and WKY rats, in which the expression of p21^WAF1/CIP1 was upregulated by 4.15-fold (P=0.002) and reversed by losartan. Surface area, protein content, mRNA and protein expressions of β-MHC, ANP and p21^WAF1/CIP1 in H9c2 cells treated with AngII elevated significantly compared with control group. p21-Ad transfection markedly increased the surface area and β-MHC mRNA expression of normal NRVMs, and p21-siRNA transfection decreased them in AngII-treated NRVMs. STE treatment decreased HW/BW and cross-sectional area, expression levels of β-MHC, ANP and p21 significantly in ISO-treated mice. Conclusion: Our findings suggest that p21 facilitates the development of cardiac hypertrophy, and regulating the expression of p21 may be an approach to attenuate hypertrophic growth of cardiomyocytes.

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“…Since increased oxidative stress is associated with arrhythmogenesis, this may act to suppress arrhythmias (1). Nardosinone, one of the major extracts from Nardostachys, has been shown to prevent angiotensin II (AngII)-induced cardiac hypertrophy in embryonic rat hearts, particularly at a concentration of ≥100 µmol/l by inhibiting the phosphatidylinositol 3-kinase (PI3K)/Akt and MEK/ERK pathways (23).…”

Section: Roles Of Individual Components Of Wxklmentioning

confidence: 99%