Apigenin potentiates the antitumor activity of 5-FU on solid Ehrlich carcinoma: Crosstalk between apoptotic and JNK-mediated autophagic cell death platforms.

摘要: Abstract Background Although 5- Fluorouracil (5-FU) has exhibited effectiveness against cancer, novel therapeutic strategies are needed to enhance its antitumor efficiency and modulate cytotoxity. Apigenin, a flavonoid present in fruits vegetables, is potent dietary phytochemical effective cancer chemoprevention. Aim This study was undertaken investigate the potential synergistic activity of apigenin 5-FU on Solid Ehrlich carcinoma (SEC). Methods Eighty Swiss albino male mice were divided into four equal groups: vehicle treated control SEC, SEC + 5-FU, SEC + apigenin, SEC + 5-FU + apigenin. Beclin-1 caspases 3, 9 JNK activities estimated by ELISA; mRNA expression levels antiapoptotic gene Mcl-1 using quantitative real-time RT-PCR, while tissue malondialdehyde (MDA), glutathione peroxidase total antioxidant capacity evaluated spectrophotometrically. A part tumor examined for histopathological Ki-67 immunohistochemistry analysis. Results and/or caused significant increase Beclin-1, activities, MDA with decrease volume, Mcl-1expression, alleviated changes proliferation index compared SEC group. In conclusion The combination had greater effect than each or alone solid mice.