Gracilaria changii derived cholesterol cause necrotic cell death in an ovarian adenocarcinoma cell line, caov-3 through p38 MAPK and fasl activation in combination with ethanol

Research output: Contribution to journalArticle

Abstract

A sterol compound found abundantly in Malaysia local red seaweed, Gracilaria changii diethyl ether fraction showed an unexpected in vitro cytotoxicity towards ovarian adenocarcinoma cell line, Caov-3, in combination with ethanol (GCM1-Et) without affecting the control cell line. Further assessment on p38 MAPK levels showed a transient expression of phosphorylated-p38 MAPK (p-p38) followed by increased expression of Fas and FasL upon treatment of GCM1-Et. In contrast to p-p38, FasL expressions were sustained until 24 hours. In the presence of p38 MAPK inhibitor (SB203580), both p-p38 MAPK and FasL signals were diminished, thus confirmed the correlation between p-p38 MAPK and increased level of FasL. Cell viability assay revealed the death of 37.8±6.87% Caov-3 cell population upon GCM1-Et treatment and was reduced to 10.5±8.03% in the presence of inhibitor. Morphology and DNA fragmentation analysis showed a dominant necrotic cell death which were characterized by high percentage of degraded chromatin without condensation (93.89%) and smearing of genomic DNA that took place upon GCM1-Et treatment. Thus, this G. changii cholesterol is believed to be responsible in inducing necrotic cell death of Caov-3 cells through increased level of p-p38 MAPK and FasL.

Original languageEnglish
Pages (from-to)1-13
Number of pages13
JournalGlobal Journal of Pharmacology
Volume7
Issue number1
DOIs
Publication statusPublished - 2013

Fingerprint

Gracilaria
p38 Mitogen-Activated Protein Kinases
Adenocarcinoma
Cell Death
Ethanol
Cholesterol
Cell Line
Seaweed
Malaysia
Sterols
DNA Fragmentation
Ether
Chromatin
Cell Survival
DNA

Keywords

  • Cholesterol
  • Gracilaria
  • Necrosis
  • Ovarian
  • p38

ASJC Scopus subject areas

  • Pharmacology, Toxicology and Pharmaceutics(all)

Cite this

@article{67eb7902dbd34daab65a5f0778e57c00,
title = "Gracilaria changii derived cholesterol cause necrotic cell death in an ovarian adenocarcinoma cell line, caov-3 through p38 MAPK and fasl activation in combination with ethanol",
abstract = "A sterol compound found abundantly in Malaysia local red seaweed, Gracilaria changii diethyl ether fraction showed an unexpected in vitro cytotoxicity towards ovarian adenocarcinoma cell line, Caov-3, in combination with ethanol (GCM1-Et) without affecting the control cell line. Further assessment on p38 MAPK levels showed a transient expression of phosphorylated-p38 MAPK (p-p38) followed by increased expression of Fas and FasL upon treatment of GCM1-Et. In contrast to p-p38, FasL expressions were sustained until 24 hours. In the presence of p38 MAPK inhibitor (SB203580), both p-p38 MAPK and FasL signals were diminished, thus confirmed the correlation between p-p38 MAPK and increased level of FasL. Cell viability assay revealed the death of 37.8±6.87{\%} Caov-3 cell population upon GCM1-Et treatment and was reduced to 10.5±8.03{\%} in the presence of inhibitor. Morphology and DNA fragmentation analysis showed a dominant necrotic cell death which were characterized by high percentage of degraded chromatin without condensation (93.89{\%}) and smearing of genomic DNA that took place upon GCM1-Et treatment. Thus, this G. changii cholesterol is believed to be responsible in inducing necrotic cell death of Caov-3 cells through increased level of p-p38 MAPK and FasL.",
keywords = "Cholesterol, Gracilaria, Necrosis, Ovarian, p38",
author = "Johari, {Nor Azfa} and {Mohd. Sidek}, Hasidah and Roohaida Othman and Nurina Anuar",
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T1 - Gracilaria changii derived cholesterol cause necrotic cell death in an ovarian adenocarcinoma cell line, caov-3 through p38 MAPK and fasl activation in combination with ethanol

AU - Johari, Nor Azfa

AU - Mohd. Sidek, Hasidah

AU - Othman, Roohaida

AU - Anuar, Nurina

PY - 2013

Y1 - 2013

N2 - A sterol compound found abundantly in Malaysia local red seaweed, Gracilaria changii diethyl ether fraction showed an unexpected in vitro cytotoxicity towards ovarian adenocarcinoma cell line, Caov-3, in combination with ethanol (GCM1-Et) without affecting the control cell line. Further assessment on p38 MAPK levels showed a transient expression of phosphorylated-p38 MAPK (p-p38) followed by increased expression of Fas and FasL upon treatment of GCM1-Et. In contrast to p-p38, FasL expressions were sustained until 24 hours. In the presence of p38 MAPK inhibitor (SB203580), both p-p38 MAPK and FasL signals were diminished, thus confirmed the correlation between p-p38 MAPK and increased level of FasL. Cell viability assay revealed the death of 37.8±6.87% Caov-3 cell population upon GCM1-Et treatment and was reduced to 10.5±8.03% in the presence of inhibitor. Morphology and DNA fragmentation analysis showed a dominant necrotic cell death which were characterized by high percentage of degraded chromatin without condensation (93.89%) and smearing of genomic DNA that took place upon GCM1-Et treatment. Thus, this G. changii cholesterol is believed to be responsible in inducing necrotic cell death of Caov-3 cells through increased level of p-p38 MAPK and FasL.

AB - A sterol compound found abundantly in Malaysia local red seaweed, Gracilaria changii diethyl ether fraction showed an unexpected in vitro cytotoxicity towards ovarian adenocarcinoma cell line, Caov-3, in combination with ethanol (GCM1-Et) without affecting the control cell line. Further assessment on p38 MAPK levels showed a transient expression of phosphorylated-p38 MAPK (p-p38) followed by increased expression of Fas and FasL upon treatment of GCM1-Et. In contrast to p-p38, FasL expressions were sustained until 24 hours. In the presence of p38 MAPK inhibitor (SB203580), both p-p38 MAPK and FasL signals were diminished, thus confirmed the correlation between p-p38 MAPK and increased level of FasL. Cell viability assay revealed the death of 37.8±6.87% Caov-3 cell population upon GCM1-Et treatment and was reduced to 10.5±8.03% in the presence of inhibitor. Morphology and DNA fragmentation analysis showed a dominant necrotic cell death which were characterized by high percentage of degraded chromatin without condensation (93.89%) and smearing of genomic DNA that took place upon GCM1-Et treatment. Thus, this G. changii cholesterol is believed to be responsible in inducing necrotic cell death of Caov-3 cells through increased level of p-p38 MAPK and FasL.

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