Inhibitory effect of alpinate Oxyphyllae fructus extracts on Ang II-induced cardiac pathological remodeling-related pathways in H9c2 cardiomyoblast cells

Chang, Yung Ming; Velmurugan, Bharath Kumar; Kuo, Wei Wen; Chen, Yueh Sheng; Ho, Tsung Jung; Tsai, Chuan Te; Ye, Chi Xin; Tsai, Chang Hai; Tsai, Fuu Jen; Huang, Chih Yang

doi:10.1016/j.biomed.2013.05.001

Cited by 79 publications

(61 citation statements)

References 30 publications

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“…The western blotting for protein expression analysis was as described previously with slight modifications . Protein concentration of the tissue was analyzed by Lowry's protein assay.…”

Section: Methodsmentioning

confidence: 99%

Overexpression of IGF‐IIRα regulates cardiac remodeling and aggravates high salt induced apoptosis and fibrosis in transgenic rats

Chang

Nithiyanantham

Kuo

et al. 2018

Environmental Toxicology

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IGF-IIR activation regulates cardiac remodeling leading to apoptosis. Here, we identified the novel IGF-IIRα (150 KDa), a truncated IGF-IIR transcript enhances cardiac apoptosis under highsalt uptake in transgenic rat model. Echocardiographic analysis revealed decline in ejection fraction and fractional shortening percentage in IGF-IIRα (TG) rats. We found that IGF-IIRα TG rats developed severe apoptosis and fibrosis as identified through TUNEL assay and Masson's trichrome staining. Importantly, the heart functioning, apoptosis, and fibrosis were significantly affected under high-salt conditions in IGF-IIRα (TG) rats. Significant upregulation of apoptosis was evident from decreased Bcl-2, p-AKT, and p-PI3K expressions with concomitant increase in Bad, cytochrome C, cleaved caspase 3 levels. We found that, IGF-IIRα highly induced tissue fibrosis through collagen accumulation (col I, col III) and up regulated various fibrotic markers such as tPA, uPA, TGF-β, and vimentin expressions. The observed upregulation of fibrosis were significantly regulated under high-salt conditions and their over regulation under IGF-IIRα over expressions shows the key role of IGF-IIRα in promoting high-salt induced fibrosis. During IGF-IIRα over expression induced cardiotoxicity, under high salt condition, and it destroys the interaction between CHIP and HSF1, which promotes the degradation of HSF1 and results in upregulation of IGF-IIR/IGF-IIRα expressions. Altogether, the study unveils novel IGF-IIRα in the regulation of cardiac apoptosis and fibrosis under high-salt diet.

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“…The western blotting for protein expression analysis was as described previously with slight modifications . Protein concentration of the tissue was analyzed by Lowry's protein assay.…”

Section: Methodsmentioning

confidence: 99%

Overexpression of IGF‐IIRα regulates cardiac remodeling and aggravates high salt induced apoptosis and fibrosis in transgenic rats

Chang

Nithiyanantham

Kuo

et al. 2018

Environmental Toxicology

Self Cite

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“…Cells were cultured in RPMI‐1640 medium supplemented with 10% fetal bovine serum (FBS), 2 mM l ‐glutamine, 100 Units/mL penicillin, and 100 μg/mL streptomycin and grown at 37°C under a humidified 5% CO 2 and 95% air at one atmosphere. The medium was changed every 2 days (Lu et al, ; Chang et al, ).…”

Section: Methodsmentioning

confidence: 99%

Benzyl isothiocyanate (BITC) induces apoptosis of GBM 8401 human brain glioblastoma multiforms cells via activation of caspase-8/Bid and the reactive oxygen species-dependent mitochondrial pathway

Shang

Shih

et al. 2015

Environ. Toxicol.

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Benzyl isothiocyanate (BITC) is one of member of the isothiocyanate family which has been shown to induce cancer cell apoptosis in many human cancer cells. In the present study, we investigated the effects of BITC on the growth of GBM 8401 human brain glioblastoma multiforms cells. Results indicated that BITC-induced cell morphological changes decreased in the percentage of viable GBM8401 cells and these effects are dose-dependent manners. Results from flow cytometric assay indicated that BITC induced sub-G1 phase and induction of apoptosis of GBM 8401 cells. Furthermore, results also showed that BITC promoted the production of reactive oxygen species (ROS) and Ca release, but decreased the mitochondrial membrane potential (ΔΨ ) and promoted caspase-8, -9, and -3 activates. After cells were pretreated with Z-IETD-FMK, Z-LEHD-FMK, and Z-DEVD-FMK (caspase-8, -9, and -3 inhibitors, respectively) led to decrease in the activities of caspase-8, -9, and -3 and increased the percentage of viable GBM 8401 cells that indicated which BITC induced cell apoptosis through caspase-dependent pathways. Western blotting indicated that BITC induced Fas, Fas-L, FADD, caspase-8, caspase -3, and pro-apoptotic protein (Bax, Bid, and Bak), but inhibited the ant-apoptotic proteins (Bcl-2 and Bcl-x) in GBM 8401 cells. Furthermore, BITC increased the release of cytochrome c, AIF, and Endo G from mitochondria that led to cell apoptosis. Results also showed that BITC increased GADD153, GRP 78, XBP-1, and ATF-6β, IRE-1α, IRE-1β, Calpain 1 and 2 in GBM 8401 cells, which is associated with ER stress. Based on these observations, we may suggest that BITC-induced apoptosis might be through Fas receptor, ROS induced ER stress, caspase-3, and mitochondrial signaling pathways. Taken together, these molecular alterations and signaling pathways offer an insight into BITC-caused growth inhibition and induced apoptotic cell death of GBM 8401 cells. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1751-1760, 2016.

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“…A549, H1355, and LLC were cultured in DMEM medium. All media were supplemented with 10% heat‐inactivated fetal calf serum (HyClone, Logan, UT, USA), 100 units/mL penicillin, 100 μg/mL streptomycin, and 2 mM l ‐glutamine at 37°C in a 5% CO 2 ‐humidified incubator (Yang et al, ; Wen et al, ; Chang et al, ; Leung et al, ; Lin et al, ).…”

Section: Methodsmentioning

confidence: 99%

Ethanol extract ofHedyotis diffusawilld upregulates G0/G1 phase arrest and induces apoptosis in human leukemia cells by modulating caspase cascade signaling and altering associated genes expression was assayed by cDNA microarray

Kuo

Yang

et al. 2014

Environ. Toxicol.

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The authors' previous study has shown that water extract of Hedyotis diffusa Willd (HDW) promoted immune response and exhibited anti-leukemic activity in BALB/c leukemic mice in vivo. In this study, the anti-proliferation effects of ethanol extract of H. diffusa Willd (EEHDW) on lung cancer cell lines (A549, H1355, and LLC), leukemia cell lines (HL-60, WEHI-3), and a mouse melanoma cell line (B16F10) in vitro were investigated. The results demonstrated that EEHDW suppressed the cell proliferation of A549, H1355, HL-60, WEHI-3, and B16F10 cells as well as reduced cell viability in a concentration-dependent manner. We found that EEHDW inhibited the cell proliferation of HL-60 cells in concentration-dependent manner. In addition, EEHDW triggered an arrest of HL-60 cells at G0/G1 phase and sub-G1 population (apoptotic cells). EEHDW provoked DNA condensation and DNA damage in HL-60 cells. The activities of caspase-3, caspase-8, and caspase-9 were elevated in EEHDW-treated HL-60 cells. DNA microarray to investigate and display the gene levels related to cell growth, signal transduction, apoptosis, cell adhesion, cell cycle, DNA damage and repair, transcription and translation was also used. These findings suggest that EEHDW may be a potential herbal medicine and therapeutic agent for the treatment of leukemia.

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Inhibitory effect of alpinate Oxyphyllae fructus extracts on Ang II-induced cardiac pathological remodeling-related pathways in H9c2 cardiomyoblast cells

Cited by 79 publications

References 30 publications

Overexpression of IGF‐IIRα regulates cardiac remodeling and aggravates high salt induced apoptosis and fibrosis in transgenic rats

Overexpression of IGF‐IIRα regulates cardiac remodeling and aggravates high salt induced apoptosis and fibrosis in transgenic rats

Benzyl isothiocyanate (BITC) induces apoptosis of GBM 8401 human brain glioblastoma multiforms cells via activation of caspase-8/Bid and the reactive oxygen species-dependent mitochondrial pathway

Ethanol extract ofHedyotis diffusawilld upregulates G0/G1 phase arrest and induces apoptosis in human leukemia cells by modulating caspase cascade signaling and altering associated genes expression was assayed by cDNA microarray

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