Rosmarinic acid failed to suppress hydrogen peroxide-mediated apoptosis but induced apoptosis of Jurkat cells which was suppressed by Bcl-2

Evangelos Kolettas; Christoforos Thomas; Eleni Leneti; Ioannis Skoufos; Christina Mbatsi; Christina Sisoula; George Manos; Angelos Evangelou

doi:10.1007/s11010-005-9064-8

Rosmarinic acid failed to suppress hydrogen peroxide-mediated apoptosis but induced apoptosis of Jurkat cells which was suppressed by Bcl-2

Evangelos Kolettas, Christoforos Thomas, Eleni Leneti, Ioannis Skoufos, Christina Mbatsi, Christina Sisoula, George Manos, Angelos Evangelou

Research output: Contribution to journal › Article › peer-review

21 Scopus citations

Abstract

Rosmarinic acid (RosA), frequently found as a secondary metabolite in herbs and medicinal plants, has exhibited antioxidative and anti-inflammatory activities. RosA was shown to inhibit the proliferation and induce apoptosis of Jurkat T cells but the mechanism of action of RosA in apoptosis remains elusive. RosA inhibited the proliferation of Jurkat cells in a dose-dependent manner by suppressing the expression of cyclin D₃ and p21^Cip1/Waf1 and up-regulating p27^Kip1. RosA induced apoptosis of Jurkat cells in a dose-dependent manner and failed to protect them from hydrogen peroxide (H₂O₂)-mediated apoptosis. Induction of apoptosis by RosA correlated with suppression of Bcl-2 but not of Bak or PUMA. Overexpression of Bcl-2 protected Jurkat cells from both H₂O₂- and RosA-induced apoptosis by altering the ratio of anti- to pro-apoptotic members of the Bcl-2 family. In conclusion, RosA inhibited Jurkat cell proliferation by altering the expression of cyclins and cyclin-dependent kinase inhibitors and induced apoptosis most likely acting through the mitochondrial pathway and possessed no anti-oxidant properties.

Original language	English (US)
Pages (from-to)	111-120
Number of pages	10
Journal	Molecular and Cellular Biochemistry
Volume	285
Issue number	1-2
DOIs	https://doi.org/10.1007/s11010-005-9064-8
State	Published - Apr 2006

Keywords

Apoptosis
Bcl-2 members
Hydrogen peroxide
Proliferation
Rosmarinic acid

ASJC Scopus subject areas

Molecular Biology
Clinical Biochemistry
Cell Biology

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10.1007/s11010-005-9064-8

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title = "Rosmarinic acid failed to suppress hydrogen peroxide-mediated apoptosis but induced apoptosis of Jurkat cells which was suppressed by Bcl-2",

abstract = "Rosmarinic acid (RosA), frequently found as a secondary metabolite in herbs and medicinal plants, has exhibited antioxidative and anti-inflammatory activities. RosA was shown to inhibit the proliferation and induce apoptosis of Jurkat T cells but the mechanism of action of RosA in apoptosis remains elusive. RosA inhibited the proliferation of Jurkat cells in a dose-dependent manner by suppressing the expression of cyclin D3 and p21Cip1/Waf1 and up-regulating p27Kip1. RosA induced apoptosis of Jurkat cells in a dose-dependent manner and failed to protect them from hydrogen peroxide (H2O2)-mediated apoptosis. Induction of apoptosis by RosA correlated with suppression of Bcl-2 but not of Bak or PUMA. Overexpression of Bcl-2 protected Jurkat cells from both H2O2- and RosA-induced apoptosis by altering the ratio of anti- to pro-apoptotic members of the Bcl-2 family. In conclusion, RosA inhibited Jurkat cell proliferation by altering the expression of cyclins and cyclin-dependent kinase inhibitors and induced apoptosis most likely acting through the mitochondrial pathway and possessed no anti-oxidant properties.",

keywords = "Apoptosis, Bcl-2 members, Hydrogen peroxide, Proliferation, Rosmarinic acid",

author = "Evangelos Kolettas and Christoforos Thomas and Eleni Leneti and Ioannis Skoufos and Christina Mbatsi and Christina Sisoula and George Manos and Angelos Evangelou",

note = "Funding Information: We are grateful to Dr. D. Galaris, University of Ioannina for kindly providing Jurkat cells and comments on the manuscript, and to Dr. D. Tang, University of Montreal, Canada for Babe-Puro/hBcl-2. This work was supported by the program grant {\textquoteleft}ARCHIMEDES{\textquoteright}, EPEAEK, co-funded by the Hellenic Ministry of Education and EU.",

year = "2006",

month = apr,

doi = "10.1007/s11010-005-9064-8",

language = "English (US)",

volume = "285",

pages = "111--120",

journal = "Molecular and Cellular Biochemistry",

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number = "1-2",

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TY - JOUR

T1 - Rosmarinic acid failed to suppress hydrogen peroxide-mediated apoptosis but induced apoptosis of Jurkat cells which was suppressed by Bcl-2

AU - Kolettas, Evangelos

AU - Thomas, Christoforos

AU - Leneti, Eleni

AU - Skoufos, Ioannis

AU - Mbatsi, Christina

AU - Sisoula, Christina

AU - Manos, George

AU - Evangelou, Angelos

N1 - Funding Information: We are grateful to Dr. D. Galaris, University of Ioannina for kindly providing Jurkat cells and comments on the manuscript, and to Dr. D. Tang, University of Montreal, Canada for Babe-Puro/hBcl-2. This work was supported by the program grant ‘ARCHIMEDES’, EPEAEK, co-funded by the Hellenic Ministry of Education and EU.

PY - 2006/4

Y1 - 2006/4

N2 - Rosmarinic acid (RosA), frequently found as a secondary metabolite in herbs and medicinal plants, has exhibited antioxidative and anti-inflammatory activities. RosA was shown to inhibit the proliferation and induce apoptosis of Jurkat T cells but the mechanism of action of RosA in apoptosis remains elusive. RosA inhibited the proliferation of Jurkat cells in a dose-dependent manner by suppressing the expression of cyclin D3 and p21Cip1/Waf1 and up-regulating p27Kip1. RosA induced apoptosis of Jurkat cells in a dose-dependent manner and failed to protect them from hydrogen peroxide (H2O2)-mediated apoptosis. Induction of apoptosis by RosA correlated with suppression of Bcl-2 but not of Bak or PUMA. Overexpression of Bcl-2 protected Jurkat cells from both H2O2- and RosA-induced apoptosis by altering the ratio of anti- to pro-apoptotic members of the Bcl-2 family. In conclusion, RosA inhibited Jurkat cell proliferation by altering the expression of cyclins and cyclin-dependent kinase inhibitors and induced apoptosis most likely acting through the mitochondrial pathway and possessed no anti-oxidant properties.

AB - Rosmarinic acid (RosA), frequently found as a secondary metabolite in herbs and medicinal plants, has exhibited antioxidative and anti-inflammatory activities. RosA was shown to inhibit the proliferation and induce apoptosis of Jurkat T cells but the mechanism of action of RosA in apoptosis remains elusive. RosA inhibited the proliferation of Jurkat cells in a dose-dependent manner by suppressing the expression of cyclin D3 and p21Cip1/Waf1 and up-regulating p27Kip1. RosA induced apoptosis of Jurkat cells in a dose-dependent manner and failed to protect them from hydrogen peroxide (H2O2)-mediated apoptosis. Induction of apoptosis by RosA correlated with suppression of Bcl-2 but not of Bak or PUMA. Overexpression of Bcl-2 protected Jurkat cells from both H2O2- and RosA-induced apoptosis by altering the ratio of anti- to pro-apoptotic members of the Bcl-2 family. In conclusion, RosA inhibited Jurkat cell proliferation by altering the expression of cyclins and cyclin-dependent kinase inhibitors and induced apoptosis most likely acting through the mitochondrial pathway and possessed no anti-oxidant properties.

KW - Apoptosis

KW - Bcl-2 members

KW - Hydrogen peroxide

KW - Proliferation

KW - Rosmarinic acid

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SN - 0300-8177

VL - 285

SP - 111

EP - 120

JO - Molecular and Cellular Biochemistry

JF - Molecular and Cellular Biochemistry

IS - 1-2

ER -

Rosmarinic acid failed to suppress hydrogen peroxide-mediated apoptosis but induced apoptosis of Jurkat cells which was suppressed by Bcl-2

Abstract

Keywords

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