The Mechanism of Intracellular Signal Pathway that Baicalin Hydrate Elevate Chemotherapeutic Response of Cervical Carcinoma.
- Author:
Byoung Ryun KIM
1
;
In Suk KIM
;
Kyoung Hee KO
;
Je Jung LEE
;
Heung Gon KIM
;
Rae Gil PARK
Author Information
1. Department of Obstetrics and Gynecology, College of Medicine, Wonkwang University, Iksan, Korea.
- Publication Type:Original Article
- Keywords:
Biacalin;
Cytotoxic effect;
HeLa cell
- MeSH:
Apoptosis;
bcl-2 Homologous Antagonist-Killer Protein;
BH3 Interacting Domain Death Agonist Protein;
Caspase 3;
Cell Death;
Chromatin;
DNA;
Flavonoids;
HeLa Cells;
Histones;
Humans;
Membrane Potential, Mitochondrial;
Phosphorylation;
Ribose;
Signal Transduction*
- From:Korean Journal of Obstetrics and Gynecology
2003;46(10):1965-1974
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Baicalin is flavonoid and major component of PC-SPES. Flavonoids including baicalin have been reported to not only function as anti-oxidant but also cause cytotoxic effect. Baicalin hydrate has been reported to induce cell death, however the mechanism by which baicalin hydrate induces the apoptosis of cancer cells is still unclear. To evaluate the mechanistic insights of apoptosis by baicalin hydrate, we tested the activities of apoptosis signaling pathway in HeLa cells. The viability of HeLa and HeLa s3 cells was markedly decreased by baicalin hydrate in a dose- and time- dependent method. Baicalin hydrate induced the apoptotic death of HeLa cells, which was characterized by the chromatin condensation of the nuclei and phosphorylation of histone H2AX. Baicalin hydrate increased the sub-G1 DNA content of HeLa cell lines. Baicalin hydrate digested Bid protein, increased Bak protein level and also, induced mitochondrial dysfunction disrupted as shown as the mitochondrial membrane potential. It activated caspase-3, thereby resulted in cleavage of poly (ADP) ribose polymerase (PARP).
