Studies on the inhibitory mechanisms of baicalein in B16F10 melanoma cell proliferation

Wen Hsien Hsu, Wei Wen Chang, Joen Rong Sheu, Y. U Kai Hsiao, Yan Jyu Tsai, Duen Suey Chou

Research output: Contribution to journalArticle

Abstract

Baicalein induces the formation of superoxide and hydroxyl radicals via 12-lipoxygenase (12-LOX) in the B16F10 mouse melanoma cell line; baicalein also causes a reduction in cellular viability and induces cell apoptosis. In this study, we utilized ROS scavengers to evaluate the role of ROS in baicalein-induced cell death and used the 12-LOX downstream product, 12-hydroxyeicosatetraenoic acid (12-HETE), to counterbalance the 12-LOX-inhibitory action of baicalein. ROS scavengers had no effect on cell differentiation, but in the cellular viability (MTT) assay, ROS scavengers effectively reversed cell viability reduction induced by baicalein. A Western blot analysis revealed that the ROS scavengers had no effect on the cell apoptosis protein, active caspase-3. From the aspect of 12-LOX, 12-HETE had no effect on cell differentiation, but it effectively reversed the reduction in cellular viability caused by baicalein in B16F10 cells. 12-HETE also possessed an inhibitory effect on the increase in expression of active caspase-3 caused by baicalein. Combined pretreatment with ROS scavengers and 12-HETE minimized the damage caused by baicalein. The majority of cell death occurring in response to baicalein-induced ROS formation in B16F10 mouse melanoma was due to cell necrosis. Cell apoptosis due to 12-LOX suppression by baicalein only accounted for a small portion.

Original languageEnglish
JournalJournal of Food and Drug Analysis
Volume19
Issue number3
Publication statusPublished - Sep 2011

Fingerprint

melanoma
lipoxygenase
Melanoma
cell proliferation
Cell Proliferation
Arachidonate 12-Lipoxygenase
Hydroxyeicosatetraenoic Acids
apoptosis
acids
viability
caspase-3
cell differentiation
cells
cell death
mice
hydroxyl radicals
Apoptosis
Caspase 3
superoxide anion
cell viability

Keywords

  • 12-Lipoxygenase
  • Apoptosis
  • B16F10 cells
  • Baicalein
  • Necrosis
  • Reactive oxygen species

ASJC Scopus subject areas

  • Food Science
  • Pharmacology

Cite this

Studies on the inhibitory mechanisms of baicalein in B16F10 melanoma cell proliferation. / Hsu, Wen Hsien; Chang, Wei Wen; Sheu, Joen Rong; Hsiao, Y. U Kai; Tsai, Yan Jyu; Chou, Duen Suey.

In: Journal of Food and Drug Analysis, Vol. 19, No. 3, 09.2011.

Research output: Contribution to journalArticle

@article{579bb2ed69a041efb20a98c678f2506a,
title = "Studies on the inhibitory mechanisms of baicalein in B16F10 melanoma cell proliferation",
abstract = "Baicalein induces the formation of superoxide and hydroxyl radicals via 12-lipoxygenase (12-LOX) in the B16F10 mouse melanoma cell line; baicalein also causes a reduction in cellular viability and induces cell apoptosis. In this study, we utilized ROS scavengers to evaluate the role of ROS in baicalein-induced cell death and used the 12-LOX downstream product, 12-hydroxyeicosatetraenoic acid (12-HETE), to counterbalance the 12-LOX-inhibitory action of baicalein. ROS scavengers had no effect on cell differentiation, but in the cellular viability (MTT) assay, ROS scavengers effectively reversed cell viability reduction induced by baicalein. A Western blot analysis revealed that the ROS scavengers had no effect on the cell apoptosis protein, active caspase-3. From the aspect of 12-LOX, 12-HETE had no effect on cell differentiation, but it effectively reversed the reduction in cellular viability caused by baicalein in B16F10 cells. 12-HETE also possessed an inhibitory effect on the increase in expression of active caspase-3 caused by baicalein. Combined pretreatment with ROS scavengers and 12-HETE minimized the damage caused by baicalein. The majority of cell death occurring in response to baicalein-induced ROS formation in B16F10 mouse melanoma was due to cell necrosis. Cell apoptosis due to 12-LOX suppression by baicalein only accounted for a small portion.",
keywords = "12-Lipoxygenase, Apoptosis, B16F10 cells, Baicalein, Necrosis, Reactive oxygen species",
author = "Hsu, {Wen Hsien} and Chang, {Wei Wen} and Sheu, {Joen Rong} and Hsiao, {Y. U Kai} and Tsai, {Yan Jyu} and Chou, {Duen Suey}",
year = "2011",
month = "9",
language = "English",
volume = "19",
journal = "Journal of Food and Drug Analysis",
issn = "1021-9498",
publisher = "Elsevier Taiwan LLC",
number = "3",

}

TY - JOUR

T1 - Studies on the inhibitory mechanisms of baicalein in B16F10 melanoma cell proliferation

AU - Hsu, Wen Hsien

AU - Chang, Wei Wen

AU - Sheu, Joen Rong

AU - Hsiao, Y. U Kai

AU - Tsai, Yan Jyu

AU - Chou, Duen Suey

PY - 2011/9

Y1 - 2011/9

N2 - Baicalein induces the formation of superoxide and hydroxyl radicals via 12-lipoxygenase (12-LOX) in the B16F10 mouse melanoma cell line; baicalein also causes a reduction in cellular viability and induces cell apoptosis. In this study, we utilized ROS scavengers to evaluate the role of ROS in baicalein-induced cell death and used the 12-LOX downstream product, 12-hydroxyeicosatetraenoic acid (12-HETE), to counterbalance the 12-LOX-inhibitory action of baicalein. ROS scavengers had no effect on cell differentiation, but in the cellular viability (MTT) assay, ROS scavengers effectively reversed cell viability reduction induced by baicalein. A Western blot analysis revealed that the ROS scavengers had no effect on the cell apoptosis protein, active caspase-3. From the aspect of 12-LOX, 12-HETE had no effect on cell differentiation, but it effectively reversed the reduction in cellular viability caused by baicalein in B16F10 cells. 12-HETE also possessed an inhibitory effect on the increase in expression of active caspase-3 caused by baicalein. Combined pretreatment with ROS scavengers and 12-HETE minimized the damage caused by baicalein. The majority of cell death occurring in response to baicalein-induced ROS formation in B16F10 mouse melanoma was due to cell necrosis. Cell apoptosis due to 12-LOX suppression by baicalein only accounted for a small portion.

AB - Baicalein induces the formation of superoxide and hydroxyl radicals via 12-lipoxygenase (12-LOX) in the B16F10 mouse melanoma cell line; baicalein also causes a reduction in cellular viability and induces cell apoptosis. In this study, we utilized ROS scavengers to evaluate the role of ROS in baicalein-induced cell death and used the 12-LOX downstream product, 12-hydroxyeicosatetraenoic acid (12-HETE), to counterbalance the 12-LOX-inhibitory action of baicalein. ROS scavengers had no effect on cell differentiation, but in the cellular viability (MTT) assay, ROS scavengers effectively reversed cell viability reduction induced by baicalein. A Western blot analysis revealed that the ROS scavengers had no effect on the cell apoptosis protein, active caspase-3. From the aspect of 12-LOX, 12-HETE had no effect on cell differentiation, but it effectively reversed the reduction in cellular viability caused by baicalein in B16F10 cells. 12-HETE also possessed an inhibitory effect on the increase in expression of active caspase-3 caused by baicalein. Combined pretreatment with ROS scavengers and 12-HETE minimized the damage caused by baicalein. The majority of cell death occurring in response to baicalein-induced ROS formation in B16F10 mouse melanoma was due to cell necrosis. Cell apoptosis due to 12-LOX suppression by baicalein only accounted for a small portion.

KW - 12-Lipoxygenase

KW - Apoptosis

KW - B16F10 cells

KW - Baicalein

KW - Necrosis

KW - Reactive oxygen species

UR - http://www.scopus.com/inward/record.url?scp=83455164097&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=83455164097&partnerID=8YFLogxK

M3 - Article

VL - 19

JO - Journal of Food and Drug Analysis

JF - Journal of Food and Drug Analysis

SN - 1021-9498

IS - 3

ER -