Korean J Obstet Gynecol.  2003 Oct;46(10):1965-1974.

The Mechanism of Intracellular Signal Pathway that Baicalin Hydrate Elevate Chemotherapeutic Response of Cervical Carcinoma

Affiliations
  • 1Department of Obstetrics and Gynecology, College of Medicine, Wonkwang University, Iksan, Korea.
  • 2Department of Microbiology, College of Medicine, Wonkwang University, Iksan, Korea.

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).

Keyword

Biacalin; Cytotoxic effect; HeLa cell

MeSH Terms

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*
BH3 Interacting Domain Death Agonist Protein
Caspase 3
Chromatin
DNA
Flavonoids
Histones
Ribose
bcl-2 Homologous Antagonist-Killer Protein
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