- Tytuł:
- Induction of ROS by a novel chromone linked nitrone derivative promotes mitochondria mediated caspase dependent apoptosis in HepG2 and HeLa cells
- Autorzy:
-
Mandal, Supratim
Mallick, Suvadip
Maiti, Sourav
Bandyopadhya, Chandrakanta
Pal, Chiranjib - Powiązania:
- https://bibliotekanauki.pl/articles/1177437.pdf
- Data publikacji:
- 2018
- Wydawca:
- Przedsiębiorstwo Wydawnictw Naukowych Darwin / Scientific Publishing House DARWIN
- Tematy:
-
Anticancer activity
Apoptosis
Caspases
Chromones
HeLa-HepG2 cell lines
Mitochondrial membrane potential
Reactive oxygen species generation - Opis:
- Chromones are organic compounds reported to induce cytotoxic effect in an extensive variety of cells. Consequently, the synthesis and reorientation of the chromone molecules are of great interest for many researchers because of their miscellaneous biological activities. The present study was designed to assess the significant antitumor effects of C-(6-Methyl-4-oxo-4H-1-benzopyran-3-yl)-N-(p-tolyl) nitrone, a novel chromone linked nitrone derivative and to elucidate the mechanism of these effects on two human cancer cell lines HepG2 and HeLa. Cell proliferation was analysed by the MTT assay. Apoptosis was evaluated by DAPI staining and flow cytometric analysis and quantified by fluorometric assays for Caspase 3 and 9. Apaf-1 and cytochrome c expression were identified by means of Western Blot analysis. The derivative showed significant dose dependent cytotoxic effects in the cancer cells and induced the reactive oxygen species and endogenous nitric oxide production. Furthermore, mitochondrial membrane potential depolarization, translocation of mitochondrial cytochrome c to cytosol, induction of Apaf-1 and activation of caspases were observed during the derivative-mediated apoptosis. These findings proposed that the novel chromone linked nitrone derivative has significant antitumor effects on HepG2 and HeLa cells and have immense scope to develop as an anticancer agent.
- Źródło:
-
World Scientific News; 2018, 103; 167-185
2392-2192 - Pojawia się w:
- World Scientific News
- Dostawca treści:
- Biblioteka Nauki
Artykuł