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The molecular mechanisms of HepG2 apoptosis induced by Hedyotis diffusa
Author(s) -
Wang ShuQing,
Kang YuMing,
Wang ShuQiu,
Lv DaMing,
Qin WenBo,
Li DianGang
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.1056.7
Subject(s) - apoptosis , cell growth , immunohistochemistry , caspase 3 , microbiology and biotechnology , chemistry , cell , viability assay , biology , programmed cell death , biochemistry , immunology
The present study was undertaken to investigate the molecular mechanisms of inhibitory effects on proliferation and apoptosis inducing effect of Hedyotis diffusa (EHD) in HepG2. The viability and proliferation of HepG2 cell co‐culturing with EHD extraction were measured by MTT. Apoptosis frequency of HepG2 cell co‐culturing with EHD extraction was detected by FCM. The expression of bcl‐2 and caspase‐3 were detected by immunohistochemical analysis. Results: EHD inhibited the growth of HepG2 cells in time and dose‐dependent way, obvious morphological and biomolecular changes of apoptosis of HepG2 cells were detected after 48h EHD treatment evidenced by microscope observation and typical DNA ladder, EHD increases the apoptotic rates of HepG2 cells in dose‐dependent way after 48h EHD treatment, immunohistochemical analysis showed that EHD decreased bcl‐2 expression and increased caspase‐3 expression in dose‐dependent way after 48h EHD treatment. EHD inhibits the proliferation of HepG2 cells and induces apoptosis of HepG2 cells which is time‐dependent and dose‐dependent way. The expression of bcl‐2 and caspase‐3 was involved in this mechanism.