Hesperidin is a
vitamin P
flavonoid compound primarily present in citrus fruits. The aim of the present study was to investigate whether
hesperidin inhibits
ovarian cancer cell viability via endoplasmic reticulum stress signaling pathways. A2780 cells were treated with various doses of
hesperidin for 6, 12 or 24 h, and the viability of A2780 cells was assessed using the MTT assay.
Hesperidin decreased the viability of A2780 cells and increased cytotoxicity in a dose- and time-dependent manner. In addition,
hesperidin induced apoptosis and increased cleaved
caspase-3 protein expression levels in A2780 cells. Furthermore,
hesperidin markedly increased the
protein expression of anti-growth arrest- and DNA damage-inducible gene 153, anti-
CCAAT'enhancer-binding protein homologous
protein,
glucose-regulated
protein 78 and
cytochrome c in A2780 cells. The results of the present study indicated that
hesperidin inhibits cell viability and induces apoptosis in
ovarian cancer cells via endoplasmic reticulum stress signaling pathways. Thus,
hesperidin may offer a novel therapeutic tool for ovarian
carcinoma.