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3,5-Dicaffeoylquinic acid protects H9C2 cells against oxidative stress-induced apoptosis via activation of the PI3K/Akt signaling pathway

Food & nutrition research, 2018-10, Vol.62, p.1-8 [Peer Reviewed Journal]

2018. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;2018 Yi-ming Bi et al. 2018 ;ISSN: 1654-661X ;EISSN: 1654-661X ;DOI: 10.29219/fnr.v62.1423 ;PMID: 30349447

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Title:
3,5-Dicaffeoylquinic acid protects H9C2 cells against oxidative stress-induced apoptosis via activation of the PI3K/Akt signaling pathway
Author: Bi, Yi-Ming ; Wu, Yu-Ting ; Chen, Ling ; Tan, Zhang-Bin ; Fan, Hui-Jie ; Xie, Ling-Peng ; Zhang, Wen-Tong ; Chen, Hong-Mei ; Li, Jun ; Liu, Bin ; Zhou, Ying-Chun
Subjects: 1-Phosphatidylinositol 3-kinase ; 3,5-dicaffeoylquinic acid ; Acids ; Activation ; AKT protein ; Apoptosis ; Bax protein ; Bcl-2 protein ; Butyl hydroperoxide ; cardiomyocyte ; Cardiomyocytes ; Cardiovascular disease ; Caspase ; Caspase-3 ; Cell lines ; Cell survival ; Chromosome 10 ; Fluorescence ; Growth factors ; Heart ; Heart diseases ; Heart failure ; Homology ; Incubation ; Inhibitors ; Iodides ; Ischemia ; Kinases ; Medical prognosis ; Mortality ; Myocardium ; Nuclei (cytology) ; Original ; Oxidative stress ; Phenols ; Phosphorylation ; PI3K/Akt pathway ; Propidium iodide ; Protein-serine/threonine kinase ; Proteins ; PTEN protein ; Signal transduction ; Signaling ; Studies ; Tensin ; Threonine
Is Part Of: Food & nutrition research, 2018-10, Vol.62, p.1-8
Description: Oxidative stress-induced apoptosis plays an important role in the development of heart failure. 3,5-Dicaffeoylquinic acid (3,5-diCQA), a phenolic compound, has shown protective effects against oxidative stress in many diseases. The objective of this study was to investigate the anti-apoptosis potential of 3,5-diCQA in cardiomyocyte cells under oxidative stress and explore its underlying mechanisms. A model of tert-butyl hydroperoxide (TBHP)-induced apoptosis in a cardiomyocyte cell line (H9C2) was established. Cell viabilities on cell lines were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium (MTT) assay. The apoptosis was measured by hoechst33342 and propidium iodide (PI) fluorescent staining. PI (in red) stained the regions of cell apoptosis; Hoechet33342 (in blue) stained the nuclei. The Western blot was used to determine the expressions of related proteins such as p-PI3K: phosphorylated phosphatidylinositol-3-kinase (p-PI3K), phosphorylated Serine and Threonine kinase AKT (p-AKT), p-PTEN, Bcl-2, Bax, and caspase-3. Afterward, a PI3K inhibitor, LY294002, was applied to confirm the influence of the PI3K/Akt pathway on TBHP-treated cells of 3,5-diCQA. Then, H9C2 cells were pre-incubated with 3,5-diCQA alone to determine if the expression of activated PI3K/Akt signaling was mediated by 3,5-diCQA in H9C2 cells. The results showed that TBHP resulted in an increase in cardiomyocyte apoptosis, whereas 3,5-diCQA treatment protected cells from TBHP-induced apoptosis in a dose-dependent manner. Moreover, 3,5-diCQA decreased expressions of Bax and caspase-3 but increased the phosphorylation levels of PI3K and Akt in TBHP-treated cells, which are the key molecules mediating cell survival, whereas phosphatase and tensin homologue deleted on chromosome 10 (PTEN) phosphorylation was unchanged. Importantly, pre-incubation with a PI3K inhibitor (LY294002) partly abolished the anti-apoptosis effects of 3,5-diCQA. Further, 3,5-diCQA enhanced the phosphorylation levels of PI3K and Akt in H9C2 cells directly, while LY294002 attenuated the effects of 3,5-diCQA on PI3K and Akt. This study suggested that 3,5-diCQA rescued myocardium from apoptosis by increasing the activation of the PI3K/Akt signaling pathway.
Publisher: Sweden: Swedish Nutrition Foundation, SNF
Language: English
Identifier: ISSN: 1654-661X
EISSN: 1654-661X
DOI: 10.29219/fnr.v62.1423
PMID: 30349447
Source: Co Action Open Access Journals
PubMed Central
ROAD: Directory of Open Access Scholarly Resources
DOAJ Directory of Open Access Journals

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3,5-Dicaffeoylquinic acid protects H9C2 cells against oxidative stress-induced apoptosis via activation of the PI3K/Akt signaling pathway

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