Plumbagin induces RPE cell cycle arrest and apoptosis via p38 MARK and PI3K/AKT/mTOR signaling pathways in PVR

Abstract Background This study aimed to explore the effects of plumbagin (PLB) on ARPE-19 cells and underlying mechanism. Methods Cultured ARPE-19 cells were treated with various concentrations (0, 5, 15, and 25 μM) of PLB for 24 h or with 15 μM PLB for 12, 24 and 48 h. Then cell viability was evalu...
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Autor*in:	Haiting Chen [verfasserIn] Huifang Wang [verfasserIn] Jianbin An [verfasserIn] Qingli Shang [verfasserIn] Jingxue Ma [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2018

Schlagwörter:	RPE Plumbagin Proliferation

Übergeordnetes Werk:	In: BMC Complementary and Alternative Medicine - BMC, 2003, 18(2018), 1, Seite 10
Übergeordnetes Werk:	volume:18 ; year:2018 ; number:1 ; pages:10

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/s12906-018-2155-3

Katalog-ID:	DOAJ069641579

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520			\|a Abstract Background This study aimed to explore the effects of plumbagin (PLB) on ARPE-19 cells and underlying mechanism. Methods Cultured ARPE-19 cells were treated with various concentrations (0, 5, 15, and 25 μM) of PLB for 24 h or with 15 μM PLB for 12, 24 and 48 h. Then cell viability was evaluated by MTT assay and DAPI staining, while apoptosis and cell cycle progression of ARPE cells were assessed by flow cytometric analysis. Furthermore, the level of main regulatory proteins was examinated by Western boltting and the expression of relative mRNA was tested by Real-Time PCR. Results PLB exhibited potent inducing effects on cell cycle arrest at G2/M phase and apoptosis of ARPE cells via the modulation of Bcl-2 family regulators in a concentration- and time-dependent manner. PLB induced inhibition of phosphatidylinositol 3-kinase (PI3K) and p38 mitogen-activated protein kinase (p38 MAPK) signaling pathways contributing to the anti-proliferative activities in ARPE cells. Conclusions This is the first report to show that PLB could inhibit the proliferation of RPE cells through down-regulation of modulatory signaling pathways. The results open new avenues for the use of PLB in prevention and treatment of proliferative vitreoretinopathy.
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allfields	10.1186/s12906-018-2155-3 doi (DE-627)DOAJ069641579 (DE-599)DOAJ019f82ee939841c2aeaf3a32575a783b DE-627 ger DE-627 rakwb eng RZ201-999 Haiting Chen verfasserin aut Plumbagin induces RPE cell cycle arrest and apoptosis via p38 MARK and PI3K/AKT/mTOR signaling pathways in PVR 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background This study aimed to explore the effects of plumbagin (PLB) on ARPE-19 cells and underlying mechanism. Methods Cultured ARPE-19 cells were treated with various concentrations (0, 5, 15, and 25 μM) of PLB for 24 h or with 15 μM PLB for 12, 24 and 48 h. Then cell viability was evaluated by MTT assay and DAPI staining, while apoptosis and cell cycle progression of ARPE cells were assessed by flow cytometric analysis. Furthermore, the level of main regulatory proteins was examinated by Western boltting and the expression of relative mRNA was tested by Real-Time PCR. Results PLB exhibited potent inducing effects on cell cycle arrest at G2/M phase and apoptosis of ARPE cells via the modulation of Bcl-2 family regulators in a concentration- and time-dependent manner. PLB induced inhibition of phosphatidylinositol 3-kinase (PI3K) and p38 mitogen-activated protein kinase (p38 MAPK) signaling pathways contributing to the anti-proliferative activities in ARPE cells. Conclusions This is the first report to show that PLB could inhibit the proliferation of RPE cells through down-regulation of modulatory signaling pathways. The results open new avenues for the use of PLB in prevention and treatment of proliferative vitreoretinopathy. RPE Plumbagin Proliferation Other systems of medicine Huifang Wang verfasserin aut Jianbin An verfasserin aut Qingli Shang verfasserin aut Jingxue Ma verfasserin aut In BMC Complementary and Alternative Medicine BMC, 2003 18(2018), 1, Seite 10 (DE-627)331018713 (DE-600)2050429-9 14726882 nnns volume:18 year:2018 number:1 pages:10 https://doi.org/10.1186/s12906-018-2155-3 kostenfrei https://doaj.org/article/019f82ee939841c2aeaf3a32575a783b kostenfrei http://link.springer.com/article/10.1186/s12906-018-2155-3 kostenfrei https://doaj.org/toc/1472-6882 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 18 2018 1 10
spelling	10.1186/s12906-018-2155-3 doi (DE-627)DOAJ069641579 (DE-599)DOAJ019f82ee939841c2aeaf3a32575a783b DE-627 ger DE-627 rakwb eng RZ201-999 Haiting Chen verfasserin aut Plumbagin induces RPE cell cycle arrest and apoptosis via p38 MARK and PI3K/AKT/mTOR signaling pathways in PVR 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background This study aimed to explore the effects of plumbagin (PLB) on ARPE-19 cells and underlying mechanism. Methods Cultured ARPE-19 cells were treated with various concentrations (0, 5, 15, and 25 μM) of PLB for 24 h or with 15 μM PLB for 12, 24 and 48 h. Then cell viability was evaluated by MTT assay and DAPI staining, while apoptosis and cell cycle progression of ARPE cells were assessed by flow cytometric analysis. Furthermore, the level of main regulatory proteins was examinated by Western boltting and the expression of relative mRNA was tested by Real-Time PCR. Results PLB exhibited potent inducing effects on cell cycle arrest at G2/M phase and apoptosis of ARPE cells via the modulation of Bcl-2 family regulators in a concentration- and time-dependent manner. PLB induced inhibition of phosphatidylinositol 3-kinase (PI3K) and p38 mitogen-activated protein kinase (p38 MAPK) signaling pathways contributing to the anti-proliferative activities in ARPE cells. Conclusions This is the first report to show that PLB could inhibit the proliferation of RPE cells through down-regulation of modulatory signaling pathways. The results open new avenues for the use of PLB in prevention and treatment of proliferative vitreoretinopathy. RPE Plumbagin Proliferation Other systems of medicine Huifang Wang verfasserin aut Jianbin An verfasserin aut Qingli Shang verfasserin aut Jingxue Ma verfasserin aut In BMC Complementary and Alternative Medicine BMC, 2003 18(2018), 1, Seite 10 (DE-627)331018713 (DE-600)2050429-9 14726882 nnns volume:18 year:2018 number:1 pages:10 https://doi.org/10.1186/s12906-018-2155-3 kostenfrei https://doaj.org/article/019f82ee939841c2aeaf3a32575a783b kostenfrei http://link.springer.com/article/10.1186/s12906-018-2155-3 kostenfrei https://doaj.org/toc/1472-6882 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 18 2018 1 10
allfields_unstemmed	10.1186/s12906-018-2155-3 doi (DE-627)DOAJ069641579 (DE-599)DOAJ019f82ee939841c2aeaf3a32575a783b DE-627 ger DE-627 rakwb eng RZ201-999 Haiting Chen verfasserin aut Plumbagin induces RPE cell cycle arrest and apoptosis via p38 MARK and PI3K/AKT/mTOR signaling pathways in PVR 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background This study aimed to explore the effects of plumbagin (PLB) on ARPE-19 cells and underlying mechanism. Methods Cultured ARPE-19 cells were treated with various concentrations (0, 5, 15, and 25 μM) of PLB for 24 h or with 15 μM PLB for 12, 24 and 48 h. Then cell viability was evaluated by MTT assay and DAPI staining, while apoptosis and cell cycle progression of ARPE cells were assessed by flow cytometric analysis. Furthermore, the level of main regulatory proteins was examinated by Western boltting and the expression of relative mRNA was tested by Real-Time PCR. Results PLB exhibited potent inducing effects on cell cycle arrest at G2/M phase and apoptosis of ARPE cells via the modulation of Bcl-2 family regulators in a concentration- and time-dependent manner. PLB induced inhibition of phosphatidylinositol 3-kinase (PI3K) and p38 mitogen-activated protein kinase (p38 MAPK) signaling pathways contributing to the anti-proliferative activities in ARPE cells. Conclusions This is the first report to show that PLB could inhibit the proliferation of RPE cells through down-regulation of modulatory signaling pathways. The results open new avenues for the use of PLB in prevention and treatment of proliferative vitreoretinopathy. RPE Plumbagin Proliferation Other systems of medicine Huifang Wang verfasserin aut Jianbin An verfasserin aut Qingli Shang verfasserin aut Jingxue Ma verfasserin aut In BMC Complementary and Alternative Medicine BMC, 2003 18(2018), 1, Seite 10 (DE-627)331018713 (DE-600)2050429-9 14726882 nnns volume:18 year:2018 number:1 pages:10 https://doi.org/10.1186/s12906-018-2155-3 kostenfrei https://doaj.org/article/019f82ee939841c2aeaf3a32575a783b kostenfrei http://link.springer.com/article/10.1186/s12906-018-2155-3 kostenfrei https://doaj.org/toc/1472-6882 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 18 2018 1 10
allfieldsGer	10.1186/s12906-018-2155-3 doi (DE-627)DOAJ069641579 (DE-599)DOAJ019f82ee939841c2aeaf3a32575a783b DE-627 ger DE-627 rakwb eng RZ201-999 Haiting Chen verfasserin aut Plumbagin induces RPE cell cycle arrest and apoptosis via p38 MARK and PI3K/AKT/mTOR signaling pathways in PVR 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background This study aimed to explore the effects of plumbagin (PLB) on ARPE-19 cells and underlying mechanism. Methods Cultured ARPE-19 cells were treated with various concentrations (0, 5, 15, and 25 μM) of PLB for 24 h or with 15 μM PLB for 12, 24 and 48 h. Then cell viability was evaluated by MTT assay and DAPI staining, while apoptosis and cell cycle progression of ARPE cells were assessed by flow cytometric analysis. Furthermore, the level of main regulatory proteins was examinated by Western boltting and the expression of relative mRNA was tested by Real-Time PCR. Results PLB exhibited potent inducing effects on cell cycle arrest at G2/M phase and apoptosis of ARPE cells via the modulation of Bcl-2 family regulators in a concentration- and time-dependent manner. PLB induced inhibition of phosphatidylinositol 3-kinase (PI3K) and p38 mitogen-activated protein kinase (p38 MAPK) signaling pathways contributing to the anti-proliferative activities in ARPE cells. Conclusions This is the first report to show that PLB could inhibit the proliferation of RPE cells through down-regulation of modulatory signaling pathways. The results open new avenues for the use of PLB in prevention and treatment of proliferative vitreoretinopathy. RPE Plumbagin Proliferation Other systems of medicine Huifang Wang verfasserin aut Jianbin An verfasserin aut Qingli Shang verfasserin aut Jingxue Ma verfasserin aut In BMC Complementary and Alternative Medicine BMC, 2003 18(2018), 1, Seite 10 (DE-627)331018713 (DE-600)2050429-9 14726882 nnns volume:18 year:2018 number:1 pages:10 https://doi.org/10.1186/s12906-018-2155-3 kostenfrei https://doaj.org/article/019f82ee939841c2aeaf3a32575a783b kostenfrei http://link.springer.com/article/10.1186/s12906-018-2155-3 kostenfrei https://doaj.org/toc/1472-6882 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 18 2018 1 10
allfieldsSound	10.1186/s12906-018-2155-3 doi (DE-627)DOAJ069641579 (DE-599)DOAJ019f82ee939841c2aeaf3a32575a783b DE-627 ger DE-627 rakwb eng RZ201-999 Haiting Chen verfasserin aut Plumbagin induces RPE cell cycle arrest and apoptosis via p38 MARK and PI3K/AKT/mTOR signaling pathways in PVR 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background This study aimed to explore the effects of plumbagin (PLB) on ARPE-19 cells and underlying mechanism. Methods Cultured ARPE-19 cells were treated with various concentrations (0, 5, 15, and 25 μM) of PLB for 24 h or with 15 μM PLB for 12, 24 and 48 h. Then cell viability was evaluated by MTT assay and DAPI staining, while apoptosis and cell cycle progression of ARPE cells were assessed by flow cytometric analysis. Furthermore, the level of main regulatory proteins was examinated by Western boltting and the expression of relative mRNA was tested by Real-Time PCR. Results PLB exhibited potent inducing effects on cell cycle arrest at G2/M phase and apoptosis of ARPE cells via the modulation of Bcl-2 family regulators in a concentration- and time-dependent manner. PLB induced inhibition of phosphatidylinositol 3-kinase (PI3K) and p38 mitogen-activated protein kinase (p38 MAPK) signaling pathways contributing to the anti-proliferative activities in ARPE cells. Conclusions This is the first report to show that PLB could inhibit the proliferation of RPE cells through down-regulation of modulatory signaling pathways. The results open new avenues for the use of PLB in prevention and treatment of proliferative vitreoretinopathy. RPE Plumbagin Proliferation Other systems of medicine Huifang Wang verfasserin aut Jianbin An verfasserin aut Qingli Shang verfasserin aut Jingxue Ma verfasserin aut In BMC Complementary and Alternative Medicine BMC, 2003 18(2018), 1, Seite 10 (DE-627)331018713 (DE-600)2050429-9 14726882 nnns volume:18 year:2018 number:1 pages:10 https://doi.org/10.1186/s12906-018-2155-3 kostenfrei https://doaj.org/article/019f82ee939841c2aeaf3a32575a783b kostenfrei http://link.springer.com/article/10.1186/s12906-018-2155-3 kostenfrei https://doaj.org/toc/1472-6882 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 18 2018 1 10
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Methods Cultured ARPE-19 cells were treated with various concentrations (0, 5, 15, and 25 μM) of PLB for 24 h or with 15 μM PLB for 12, 24 and 48 h. Then cell viability was evaluated by MTT assay and DAPI staining, while apoptosis and cell cycle progression of ARPE cells were assessed by flow cytometric analysis. Furthermore, the level of main regulatory proteins was examinated by Western boltting and the expression of relative mRNA was tested by Real-Time PCR. Results PLB exhibited potent inducing effects on cell cycle arrest at G2/M phase and apoptosis of ARPE cells via the modulation of Bcl-2 family regulators in a concentration- and time-dependent manner. PLB induced inhibition of phosphatidylinositol 3-kinase (PI3K) and p38 mitogen-activated protein kinase (p38 MAPK) signaling pathways contributing to the anti-proliferative activities in ARPE cells. Conclusions This is the first report to show that PLB could inhibit the proliferation of RPE cells through down-regulation of modulatory signaling pathways. The results open new avenues for the use of PLB in prevention and treatment of proliferative vitreoretinopathy.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">RPE</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Plumbagin</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Proliferation</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Other systems of medicine</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Huifang Wang</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Jianbin An</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Qingli Shang</subfield><subfield code="e">verfasserin</subfield><subfield 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callnumber-first	R - Medicine
author	Haiting Chen
spellingShingle	Haiting Chen misc RZ201-999 misc RPE misc Plumbagin misc Proliferation misc Other systems of medicine Plumbagin induces RPE cell cycle arrest and apoptosis via p38 MARK and PI3K/AKT/mTOR signaling pathways in PVR
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topic_title	RZ201-999 Plumbagin induces RPE cell cycle arrest and apoptosis via p38 MARK and PI3K/AKT/mTOR signaling pathways in PVR RPE Plumbagin Proliferation
topic	misc RZ201-999 misc RPE misc Plumbagin misc Proliferation misc Other systems of medicine
topic_unstemmed	misc RZ201-999 misc RPE misc Plumbagin misc Proliferation misc Other systems of medicine
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title	Plumbagin induces RPE cell cycle arrest and apoptosis via p38 MARK and PI3K/AKT/mTOR signaling pathways in PVR
ctrlnum	(DE-627)DOAJ069641579 (DE-599)DOAJ019f82ee939841c2aeaf3a32575a783b
title_full	Plumbagin induces RPE cell cycle arrest and apoptosis via p38 MARK and PI3K/AKT/mTOR signaling pathways in PVR
author_sort	Haiting Chen
journal	BMC Complementary and Alternative Medicine
journalStr	BMC Complementary and Alternative Medicine
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container_start_page	10
author_browse	Haiting Chen Huifang Wang Jianbin An Qingli Shang Jingxue Ma
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author-letter	Haiting Chen
doi_str_mv	10.1186/s12906-018-2155-3
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title_sort	plumbagin induces rpe cell cycle arrest and apoptosis via p38 mark and pi3k/akt/mtor signaling pathways in pvr
callnumber	RZ201-999
title_auth	Plumbagin induces RPE cell cycle arrest and apoptosis via p38 MARK and PI3K/AKT/mTOR signaling pathways in PVR
abstract	Abstract Background This study aimed to explore the effects of plumbagin (PLB) on ARPE-19 cells and underlying mechanism. Methods Cultured ARPE-19 cells were treated with various concentrations (0, 5, 15, and 25 μM) of PLB for 24 h or with 15 μM PLB for 12, 24 and 48 h. Then cell viability was evaluated by MTT assay and DAPI staining, while apoptosis and cell cycle progression of ARPE cells were assessed by flow cytometric analysis. Furthermore, the level of main regulatory proteins was examinated by Western boltting and the expression of relative mRNA was tested by Real-Time PCR. Results PLB exhibited potent inducing effects on cell cycle arrest at G2/M phase and apoptosis of ARPE cells via the modulation of Bcl-2 family regulators in a concentration- and time-dependent manner. PLB induced inhibition of phosphatidylinositol 3-kinase (PI3K) and p38 mitogen-activated protein kinase (p38 MAPK) signaling pathways contributing to the anti-proliferative activities in ARPE cells. Conclusions This is the first report to show that PLB could inhibit the proliferation of RPE cells through down-regulation of modulatory signaling pathways. The results open new avenues for the use of PLB in prevention and treatment of proliferative vitreoretinopathy.
abstractGer	Abstract Background This study aimed to explore the effects of plumbagin (PLB) on ARPE-19 cells and underlying mechanism. Methods Cultured ARPE-19 cells were treated with various concentrations (0, 5, 15, and 25 μM) of PLB for 24 h or with 15 μM PLB for 12, 24 and 48 h. Then cell viability was evaluated by MTT assay and DAPI staining, while apoptosis and cell cycle progression of ARPE cells were assessed by flow cytometric analysis. Furthermore, the level of main regulatory proteins was examinated by Western boltting and the expression of relative mRNA was tested by Real-Time PCR. Results PLB exhibited potent inducing effects on cell cycle arrest at G2/M phase and apoptosis of ARPE cells via the modulation of Bcl-2 family regulators in a concentration- and time-dependent manner. PLB induced inhibition of phosphatidylinositol 3-kinase (PI3K) and p38 mitogen-activated protein kinase (p38 MAPK) signaling pathways contributing to the anti-proliferative activities in ARPE cells. Conclusions This is the first report to show that PLB could inhibit the proliferation of RPE cells through down-regulation of modulatory signaling pathways. The results open new avenues for the use of PLB in prevention and treatment of proliferative vitreoretinopathy.
abstract_unstemmed	Abstract Background This study aimed to explore the effects of plumbagin (PLB) on ARPE-19 cells and underlying mechanism. Methods Cultured ARPE-19 cells were treated with various concentrations (0, 5, 15, and 25 μM) of PLB for 24 h or with 15 μM PLB for 12, 24 and 48 h. Then cell viability was evaluated by MTT assay and DAPI staining, while apoptosis and cell cycle progression of ARPE cells were assessed by flow cytometric analysis. Furthermore, the level of main regulatory proteins was examinated by Western boltting and the expression of relative mRNA was tested by Real-Time PCR. Results PLB exhibited potent inducing effects on cell cycle arrest at G2/M phase and apoptosis of ARPE cells via the modulation of Bcl-2 family regulators in a concentration- and time-dependent manner. PLB induced inhibition of phosphatidylinositol 3-kinase (PI3K) and p38 mitogen-activated protein kinase (p38 MAPK) signaling pathways contributing to the anti-proliferative activities in ARPE cells. Conclusions This is the first report to show that PLB could inhibit the proliferation of RPE cells through down-regulation of modulatory signaling pathways. The results open new avenues for the use of PLB in prevention and treatment of proliferative vitreoretinopathy.
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title_short	Plumbagin induces RPE cell cycle arrest and apoptosis via p38 MARK and PI3K/AKT/mTOR signaling pathways in PVR
url	https://doi.org/10.1186/s12906-018-2155-3 https://doaj.org/article/019f82ee939841c2aeaf3a32575a783b http://link.springer.com/article/10.1186/s12906-018-2155-3 https://doaj.org/toc/1472-6882
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author2	Huifang Wang Jianbin An Qingli Shang Jingxue Ma
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up_date	2024-07-04T00:06:34.709Z
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