Polyphenols from Broussonetia papyrifera Induce Apoptosis of HepG2 Cells via Inactivation of ERK and AKT Signaling Pathways | Zendy

Dou Chenzhuo | Zendy; Yanfen Liu | Zendy; Lulu Zhang | Zendy; Shaohong Chen | Zendy; Chuan-Yin Hu | Zendy; You Liu | Zendy; YunTao Zhao | Zendy

Open Access

Polyphenols from Broussonetia papyrifera Induce Apoptosis of HepG2 Cells via Inactivation of ERK and AKT Signaling Pathways

Author(s) -

Dou Chenzhuo,

Yanfen Liu,

Lulu Zhang,

Shaohong Chen,

Chuan-Yin Hu,

You Liu,

YunTao Zhao

Publication year - 2021

Publication title -

evidence-based complementary and alternative medicine

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.552

H-Index - 90

eISSN - 1741-4288

pISSN - 1741-427X

DOI - 10.1155/2021/8841706

Subject(s) - protein kinase b , mapk/erk pathway , apoptosis , chemistry , microbiology and biotechnology , intracellular , signal transduction , kinase , reactive oxygen species , biochemistry , biology

The extract of Broussonetia papyrifera has been proved to have antitumor activity. However, the underlying mechanism remains unclear. This study aimed to elucidate the mechanism of apoptosis of HepG2 cells induced by polyphenols from Broussonetia papyrifera (PBPs). The results revealed that PBPs inhibited the proliferation of HepG2 cells in a dose-dependent and time-dependent manner. Flow cytometry analysis showed that PBPs increased the apoptosis ratio of HepG2 cells significantly. PBPs increased intracellular reactive oxygen species (ROS) production and decreased intracellular superoxide dismutase (SOD) level of HepG2 cells. PBPs induced cell cycle arrest at G1 phase. Western blotting showed that PBPs upregulated the ratio of Bax / Bcl -2 and the expression level of Caspase -3, and activated p 53 in HepG2 cells. The inhibition of proliferative relative signals (protein kinase B, PKB/AKT) and survival relative signals (extracellular signal-regulated kinase, ERK) were also observed in PBP-treated HepG2 cells. Our findings suggest that apoptosis of HepG2 cells induced by PBPs is mitochondria-mediated via inactivation of ERK and AKT signaling pathways.

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