Mechanism of Taiwan Mingjian Oolong Tea to Inhibit Isoproterenol-Induced Hypertrophy and Apoptosis in Cardiomyoblasts

Yeh, Yu Lan; Tsai, Hsiang I.; Cheng, Shiu-Min; Pai, Peiying; Ho, Tsung Jung; Chen, Ray Jade; Lai, Chao Hung; Pei, Huang; Padma, Viswanadha Vijaya; Huang, Chih Yang

doi:10.1142/s0192415x16500051

Cited by 10 publications

(4 citation statements)

References 31 publications

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“…H9c2 cells are derived from embryonic rat heart tissue and exhibit many properties of skeletal muscle. These cells have long been used as a cardiac cell model in a vast number of cardiac hypertrophy studies (Yeh et al 2016;Guan et al 2017). Briefly, H9c2 cells were cultured in Dulbecco's Modified Eagle's Medium (DMEM, Gibco, Carlsbad, CA) supplemented with 10% foetal bovine serum and 100 IU/mL penicillin/streptomycin.…”

Section: Cell Culture and Treatmentmentioning

confidence: 99%

Dendrobium candidum aqueous extract attenuates isoproterenol-induced cardiac hypertrophy through the ERK signalling pathway

Cao

et al. 2020

Pharmaceutical Biology

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Context:The pharmacological functions of Dendrobium candidum Wall. ex Lindl. (Orchidaceae) in cardiac hypertrophy remains unclear. Objective: To evaluate whether D. candidum aqueous extract (DCAE) can attenuate experimental cardiac hypertrophy. Materials and methods: Cardiac hypertrophy in SD rats was induced by subcutaneously injection of isoproterenol (2 mg/kg), once a day for ten days. Rats were gavaged with DCAE (0.13 and 0.78 g/kg) daily for one month. At the end of treatment, measurement of left ventricular systolic pressure (LVSP), heartto-body weight ratio (HW/BW), left ventricular/tibia length (LV/TL), atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) levels, haematoxylin-eosin staining, and Masson's trichrome staining were conducted. In cultured H9c2 cells, DCAE (2 mg/mL) and U0126 (10 lM) were added 2 h before the isoproterenol (10 lM) stimulus. Phalloidin staining was used to evaluate cellular hypertrophy. The mRNA expression of ANP and BNP was measured by qRT-PCR. The expression of p-ERK was determined by immunoblotting. Results: DCAE treatment significantly reduced the following indicators in vivo: (1) the LVSP (16%); (2) HW/BW (13%); (3) LV/TL (6%); ( 4) ANP (39%); ( 5) BNP (32%). In cultured H9c2 cells, phalloidin staining showed that DCAE relieved cellular hypertrophy (53% reduction). Furthermore, immunoblotting showed that DCAE can significantly inhibit p-ERK protein expression in vivo and in vitro (39% and 27% reduction, respectively). Discussion and conclusions: DCAE prevents cardiac hypertrophy via ERK signalling pathway and has the potential for treatment of cardiac hypertrophy.

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Section: Cell Culture and Treatmentmentioning

confidence: 99%

Dendrobium candidum aqueous extract attenuates isoproterenol-induced cardiac hypertrophy through the ERK signalling pathway

Cao

et al. 2020

Pharmaceutical Biology

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“…Activated caspase‐8 then cleaves BH3 interacting domain death (Bid) into t‐Bid, which stimulates instability in the outer mitochondrial membrane, leading to the release of cytochrome‐c into the cytosol. Once in the cytosol, cytochrome c activates caspase‐9, which then further cleaves and activates caspase‐3, causing the induction of apoptosis …”

Section: Introductionmentioning

confidence: 99%

Preventive effect of apigenin against isoproterenol‐induced apoptosis in cardiomyoblasts

Radhiga

Robert

Sundaresan

et al. 2018

J Biochem & Molecular Tox

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We investigated the effect of apigenin, a dietary flavonoid, on isoproterenol hydrochloride (ISO)-induced apoptotic signaling in cardiomyoblast H9C2 cells. The results showed that apigenin treatment (10 µM) prevented ISO (31.25 μM)-induced lipid peroxidative levels and antioxidants status in H9C2 cells. Furthermore, apigenin inhibited expression of inflammatory markers in ISO-treated cells. In addition, apigenin prevented ISO-induced DNA damage and apoptotic signaling through modulating the expression of Bax, caspase-3, -8 and -9, cytochrome c, and Fas proteins in H9C2 cells. It is concluded that apigenin prevents ISO-induced antioxidants depletion, oxidative DNA damage, inflammatory, and apoptotic signaling in H9C2 cells. Thus, the present results demonstrated that apigenin has a cardioprotective effect on cardiomyoblasts cells.

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“…Combined with the results from the present CCK-8 assay, 40 µM was selected as the concentration to induce MH for subsequent experimentation in the present study. It has been reported that the early stage of MH is characterized by the increase of the surface area of cardiomyocytes (65). Changes in cell surface area (quantified and analyzed using immunofluorescence) directly reflect progression of cardiac hypertrophy; this method is used to assess MH.…”

Section: Discussionmentioning

confidence: 99%

Puerarin attenuates isoproterenol‑induced myocardial hypertrophy via inhibition of the Wnt/β‑catenin signaling pathway

Wang

et al. 2022

Mol Med Rep

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Myocardial hypertrophy (MH) is an independent risk factor for cardiovascular disease, which in turn lead to arrhythmia or heart failure. Therefore, attention must be paid to formulation of therapeutic strategies for MH. Puerarin is a key bioactive ingredient isolated from Pueraria genera of plants that is beneficial for the treatment of MH. However, its molecular mechanism of action has not been fully determined.In the present study, 40 µM puerarin was demonstrated to be a safe dose for human AC16 cells using Cell Counting Kit-8 assay. The protective effects of puerarin against MH were demonstrated in AC16 cells stimulated with isoproterenol (ISO). These effects were characterized by a significant decrease in surface area of cells (assessed using fluorescence staining) and mRNA and protein expression levels of MH-associated biomarkers, including atrial and brain natriuretic peptide, assessed using reverse transcription-quantitative PCR and western blotting, as well as β-myosin heavy chain mRNA expression levels. Mechanistically, western blotting demonstrated that puerarin inhibited activation of the Wnt signaling pathway. Puerarin also significantly decreased phosphorylation of p65; this was mediated via crosstalk between the Wnt and NF-κB signaling pathways. An inhibitor (Dickkopf-1) and activator (IM-12) of the Wnt signaling pathway were used to demonstrate that puerarin-mediated effects alleviated ISO-induced MH via the Wnt signaling pathway. The results of the present study demonstrated that puerarin pre-treatment may be a potential therapeutic strategy for preventing ISO-induced MH and managing MH in the future.

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Mechanism of Taiwan Mingjian Oolong Tea to Inhibit Isoproterenol-Induced Hypertrophy and Apoptosis in Cardiomyoblasts

Cited by 10 publications

References 31 publications

Dendrobium candidum aqueous extract attenuates isoproterenol-induced cardiac hypertrophy through the ERK signalling pathway

Dendrobium candidum aqueous extract attenuates isoproterenol-induced cardiac hypertrophy through the ERK signalling pathway

Preventive effect of apigenin against isoproterenol‐induced apoptosis in cardiomyoblasts

Puerarin attenuates isoproterenol‑induced myocardial hypertrophy via inhibition of the Wnt/β‑catenin signaling pathway

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