Modulation of Radiation-Induced NADPH Oxidases in Rat’s Heart Tissues by Melatonin

Background: Experimental studies have shown that infiltration of inflammatory cells as well as upregulation of some cytokines play a central role in the development of late effects of ionizing radiation in heart tissues. Evidences have shown that an increased level of TGF-β has a direct correlation...
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Autor*in:	Tayebeh Aryafar [verfasserIn] Peyman Amini [verfasserIn] Saeed Rezapoor [verfasserIn] Dheyauldeen Shabeeb [verfasserIn] Ahmed Eleojo Musa [verfasserIn] Masoud Najafi [verfasserIn] Alireza Shirazi [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	radiation melatonin heart nadph oxidase 2 nadph oxidase 4

Übergeordnetes Werk:	In: Journal of Biomedical Physics and Engineering - Shiraz University of Medical Sciences, 2012, 11(2021), 4, Seite 465-472
Übergeordnetes Werk:	volume:11 ; year:2021 ; number:4 ; pages:465-472

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.31661/jbpe.v0i0.1094

Katalog-ID:	DOAJ057351813

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520			\|a Background: Experimental studies have shown that infiltration of inflammatory cells as well as upregulation of some cytokines play a central role in the development of late effects of ionizing radiation in heart tissues. Evidences have shown that an increased level of TGF-β has a direct correlation with late effects of exposure to ionizing radiation such as chronic oxidative stress and fibrosis. Recent studies have shown that TGF-β, through upregulation of pro-oxidant enzymes such as NOX2 and NOX4, promotes continuous ROS production and accumulation of fibrosis. Objective: In present study, we aimed to evaluate the expression of NOX2 and NOX4 signaling pathways as well as possible modulatory effects of melatonin on the expression of these genes.Material and Methods: In this experimental study, four groups of 20 rats (5 in each) were used as follows; G1: control; G2: melatonin; G3: radiation; G4: radiation + melatonin. 100 mg/kg of melatonin was administrated before irradiation of heart tissues with 15 Gy gamma rays. 10 weeks after irradiation, heart tissues were collected for real-time PCR. Results: Results showed a significant increase in the expression of TGF-β, Smad2, NF-kB, NOX2 and NOX4. The upregulation of NOX2 was more obvious by 20-fold compared to other genes. Except for TGF-β, melatonin could attenuate the expression of other genes. Conclusion: This study indicated that exposure of rat’s heart tissues to radiation leads to upregulation of TGF-β-NOX4 and TGF-β-NOX2 pathways. Melatonin, through modulation of these genes, may be able to alleviate radiation-induced chronic oxidative stress and subsequent consequences.
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653		0	\|a Medical physics. Medical radiology. Nuclear medicine
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spelling	10.31661/jbpe.v0i0.1094 doi (DE-627)DOAJ057351813 (DE-599)DOAJ3f5217c4c38a419591d1bb5f5aa6f691 DE-627 ger DE-627 rakwb eng R895-920 Tayebeh Aryafar verfasserin aut Modulation of Radiation-Induced NADPH Oxidases in Rat’s Heart Tissues by Melatonin 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Experimental studies have shown that infiltration of inflammatory cells as well as upregulation of some cytokines play a central role in the development of late effects of ionizing radiation in heart tissues. Evidences have shown that an increased level of TGF-β has a direct correlation with late effects of exposure to ionizing radiation such as chronic oxidative stress and fibrosis. Recent studies have shown that TGF-β, through upregulation of pro-oxidant enzymes such as NOX2 and NOX4, promotes continuous ROS production and accumulation of fibrosis. Objective: In present study, we aimed to evaluate the expression of NOX2 and NOX4 signaling pathways as well as possible modulatory effects of melatonin on the expression of these genes.Material and Methods: In this experimental study, four groups of 20 rats (5 in each) were used as follows; G1: control; G2: melatonin; G3: radiation; G4: radiation + melatonin. 100 mg/kg of melatonin was administrated before irradiation of heart tissues with 15 Gy gamma rays. 10 weeks after irradiation, heart tissues were collected for real-time PCR. Results: Results showed a significant increase in the expression of TGF-β, Smad2, NF-kB, NOX2 and NOX4. The upregulation of NOX2 was more obvious by 20-fold compared to other genes. Except for TGF-β, melatonin could attenuate the expression of other genes. Conclusion: This study indicated that exposure of rat’s heart tissues to radiation leads to upregulation of TGF-β-NOX4 and TGF-β-NOX2 pathways. Melatonin, through modulation of these genes, may be able to alleviate radiation-induced chronic oxidative stress and subsequent consequences. radiation melatonin heart nadph oxidase 2 nadph oxidase 4 Medical physics. Medical radiology. Nuclear medicine Peyman Amini verfasserin aut Saeed Rezapoor verfasserin aut Dheyauldeen Shabeeb verfasserin aut Ahmed Eleojo Musa verfasserin aut Masoud Najafi verfasserin aut Alireza Shirazi verfasserin aut In Journal of Biomedical Physics and Engineering Shiraz University of Medical Sciences, 2012 11(2021), 4, Seite 465-472 (DE-627)720166152 (DE-600)2673599-4 22517200 nnns volume:11 year:2021 number:4 pages:465-472 https://doi.org/10.31661/jbpe.v0i0.1094 kostenfrei https://doaj.org/article/3f5217c4c38a419591d1bb5f5aa6f691 kostenfrei https://jbpe.sums.ac.ir/article_46520_bf6bec5a2a33153f054d9bfeea4e423d.pdf kostenfrei https://doaj.org/toc/2251-7200 Journal toc kostenfrei https://doaj.org/toc/2251-7200 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 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_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2055 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_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2021 4 465-472
allfields_unstemmed	10.31661/jbpe.v0i0.1094 doi (DE-627)DOAJ057351813 (DE-599)DOAJ3f5217c4c38a419591d1bb5f5aa6f691 DE-627 ger DE-627 rakwb eng R895-920 Tayebeh Aryafar verfasserin aut Modulation of Radiation-Induced NADPH Oxidases in Rat’s Heart Tissues by Melatonin 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Experimental studies have shown that infiltration of inflammatory cells as well as upregulation of some cytokines play a central role in the development of late effects of ionizing radiation in heart tissues. Evidences have shown that an increased level of TGF-β has a direct correlation with late effects of exposure to ionizing radiation such as chronic oxidative stress and fibrosis. Recent studies have shown that TGF-β, through upregulation of pro-oxidant enzymes such as NOX2 and NOX4, promotes continuous ROS production and accumulation of fibrosis. Objective: In present study, we aimed to evaluate the expression of NOX2 and NOX4 signaling pathways as well as possible modulatory effects of melatonin on the expression of these genes.Material and Methods: In this experimental study, four groups of 20 rats (5 in each) were used as follows; G1: control; G2: melatonin; G3: radiation; G4: radiation + melatonin. 100 mg/kg of melatonin was administrated before irradiation of heart tissues with 15 Gy gamma rays. 10 weeks after irradiation, heart tissues were collected for real-time PCR. Results: Results showed a significant increase in the expression of TGF-β, Smad2, NF-kB, NOX2 and NOX4. The upregulation of NOX2 was more obvious by 20-fold compared to other genes. Except for TGF-β, melatonin could attenuate the expression of other genes. Conclusion: This study indicated that exposure of rat’s heart tissues to radiation leads to upregulation of TGF-β-NOX4 and TGF-β-NOX2 pathways. Melatonin, through modulation of these genes, may be able to alleviate radiation-induced chronic oxidative stress and subsequent consequences. radiation melatonin heart nadph oxidase 2 nadph oxidase 4 Medical physics. Medical radiology. Nuclear medicine Peyman Amini verfasserin aut Saeed Rezapoor verfasserin aut Dheyauldeen Shabeeb verfasserin aut Ahmed Eleojo Musa verfasserin aut Masoud Najafi verfasserin aut Alireza Shirazi verfasserin aut In Journal of Biomedical Physics and Engineering Shiraz University of Medical Sciences, 2012 11(2021), 4, Seite 465-472 (DE-627)720166152 (DE-600)2673599-4 22517200 nnns volume:11 year:2021 number:4 pages:465-472 https://doi.org/10.31661/jbpe.v0i0.1094 kostenfrei https://doaj.org/article/3f5217c4c38a419591d1bb5f5aa6f691 kostenfrei https://jbpe.sums.ac.ir/article_46520_bf6bec5a2a33153f054d9bfeea4e423d.pdf kostenfrei https://doaj.org/toc/2251-7200 Journal toc kostenfrei https://doaj.org/toc/2251-7200 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 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_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2055 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_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2021 4 465-472
allfieldsGer	10.31661/jbpe.v0i0.1094 doi (DE-627)DOAJ057351813 (DE-599)DOAJ3f5217c4c38a419591d1bb5f5aa6f691 DE-627 ger DE-627 rakwb eng R895-920 Tayebeh Aryafar verfasserin aut Modulation of Radiation-Induced NADPH Oxidases in Rat’s Heart Tissues by Melatonin 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Experimental studies have shown that infiltration of inflammatory cells as well as upregulation of some cytokines play a central role in the development of late effects of ionizing radiation in heart tissues. Evidences have shown that an increased level of TGF-β has a direct correlation with late effects of exposure to ionizing radiation such as chronic oxidative stress and fibrosis. Recent studies have shown that TGF-β, through upregulation of pro-oxidant enzymes such as NOX2 and NOX4, promotes continuous ROS production and accumulation of fibrosis. Objective: In present study, we aimed to evaluate the expression of NOX2 and NOX4 signaling pathways as well as possible modulatory effects of melatonin on the expression of these genes.Material and Methods: In this experimental study, four groups of 20 rats (5 in each) were used as follows; G1: control; G2: melatonin; G3: radiation; G4: radiation + melatonin. 100 mg/kg of melatonin was administrated before irradiation of heart tissues with 15 Gy gamma rays. 10 weeks after irradiation, heart tissues were collected for real-time PCR. Results: Results showed a significant increase in the expression of TGF-β, Smad2, NF-kB, NOX2 and NOX4. The upregulation of NOX2 was more obvious by 20-fold compared to other genes. Except for TGF-β, melatonin could attenuate the expression of other genes. Conclusion: This study indicated that exposure of rat’s heart tissues to radiation leads to upregulation of TGF-β-NOX4 and TGF-β-NOX2 pathways. Melatonin, through modulation of these genes, may be able to alleviate radiation-induced chronic oxidative stress and subsequent consequences. radiation melatonin heart nadph oxidase 2 nadph oxidase 4 Medical physics. Medical radiology. Nuclear medicine Peyman Amini verfasserin aut Saeed Rezapoor verfasserin aut Dheyauldeen Shabeeb verfasserin aut Ahmed Eleojo Musa verfasserin aut Masoud Najafi verfasserin aut Alireza Shirazi verfasserin aut In Journal of Biomedical Physics and Engineering Shiraz University of Medical Sciences, 2012 11(2021), 4, Seite 465-472 (DE-627)720166152 (DE-600)2673599-4 22517200 nnns volume:11 year:2021 number:4 pages:465-472 https://doi.org/10.31661/jbpe.v0i0.1094 kostenfrei https://doaj.org/article/3f5217c4c38a419591d1bb5f5aa6f691 kostenfrei https://jbpe.sums.ac.ir/article_46520_bf6bec5a2a33153f054d9bfeea4e423d.pdf kostenfrei https://doaj.org/toc/2251-7200 Journal toc kostenfrei https://doaj.org/toc/2251-7200 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 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_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2055 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_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2021 4 465-472
allfieldsSound	10.31661/jbpe.v0i0.1094 doi (DE-627)DOAJ057351813 (DE-599)DOAJ3f5217c4c38a419591d1bb5f5aa6f691 DE-627 ger DE-627 rakwb eng R895-920 Tayebeh Aryafar verfasserin aut Modulation of Radiation-Induced NADPH Oxidases in Rat’s Heart Tissues by Melatonin 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Experimental studies have shown that infiltration of inflammatory cells as well as upregulation of some cytokines play a central role in the development of late effects of ionizing radiation in heart tissues. Evidences have shown that an increased level of TGF-β has a direct correlation with late effects of exposure to ionizing radiation such as chronic oxidative stress and fibrosis. Recent studies have shown that TGF-β, through upregulation of pro-oxidant enzymes such as NOX2 and NOX4, promotes continuous ROS production and accumulation of fibrosis. Objective: In present study, we aimed to evaluate the expression of NOX2 and NOX4 signaling pathways as well as possible modulatory effects of melatonin on the expression of these genes.Material and Methods: In this experimental study, four groups of 20 rats (5 in each) were used as follows; G1: control; G2: melatonin; G3: radiation; G4: radiation + melatonin. 100 mg/kg of melatonin was administrated before irradiation of heart tissues with 15 Gy gamma rays. 10 weeks after irradiation, heart tissues were collected for real-time PCR. Results: Results showed a significant increase in the expression of TGF-β, Smad2, NF-kB, NOX2 and NOX4. The upregulation of NOX2 was more obvious by 20-fold compared to other genes. Except for TGF-β, melatonin could attenuate the expression of other genes. Conclusion: This study indicated that exposure of rat’s heart tissues to radiation leads to upregulation of TGF-β-NOX4 and TGF-β-NOX2 pathways. Melatonin, through modulation of these genes, may be able to alleviate radiation-induced chronic oxidative stress and subsequent consequences. radiation melatonin heart nadph oxidase 2 nadph oxidase 4 Medical physics. Medical radiology. Nuclear medicine Peyman Amini verfasserin aut Saeed Rezapoor verfasserin aut Dheyauldeen Shabeeb verfasserin aut Ahmed Eleojo Musa verfasserin aut Masoud Najafi verfasserin aut Alireza Shirazi verfasserin aut In Journal of Biomedical Physics and Engineering Shiraz University of Medical Sciences, 2012 11(2021), 4, Seite 465-472 (DE-627)720166152 (DE-600)2673599-4 22517200 nnns volume:11 year:2021 number:4 pages:465-472 https://doi.org/10.31661/jbpe.v0i0.1094 kostenfrei https://doaj.org/article/3f5217c4c38a419591d1bb5f5aa6f691 kostenfrei https://jbpe.sums.ac.ir/article_46520_bf6bec5a2a33153f054d9bfeea4e423d.pdf kostenfrei https://doaj.org/toc/2251-7200 Journal toc kostenfrei https://doaj.org/toc/2251-7200 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 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_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2055 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_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2021 4 465-472
language	English
source	In Journal of Biomedical Physics and Engineering 11(2021), 4, Seite 465-472 volume:11 year:2021 number:4 pages:465-472
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topic_facet	radiation melatonin heart nadph oxidase 2 nadph oxidase 4 Medical physics. Medical radiology. Nuclear medicine
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authorswithroles_txt_mv	Tayebeh Aryafar @@aut@@ Peyman Amini @@aut@@ Saeed Rezapoor @@aut@@ Dheyauldeen Shabeeb @@aut@@ Ahmed Eleojo Musa @@aut@@ Masoud Najafi @@aut@@ Alireza Shirazi @@aut@@
publishDateDaySort_date	2021-01-01T00:00:00Z
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callnumber-first	R - Medicine
author	Tayebeh Aryafar
spellingShingle	Tayebeh Aryafar misc R895-920 misc radiation misc melatonin misc heart misc nadph oxidase 2 misc nadph oxidase 4 misc Medical physics. Medical radiology. Nuclear medicine Modulation of Radiation-Induced NADPH Oxidases in Rat’s Heart Tissues by Melatonin
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issn	22517200
topic_title	R895-920 Modulation of Radiation-Induced NADPH Oxidases in Rat’s Heart Tissues by Melatonin radiation melatonin heart nadph oxidase 2 nadph oxidase 4
topic	misc R895-920 misc radiation misc melatonin misc heart misc nadph oxidase 2 misc nadph oxidase 4 misc Medical physics. Medical radiology. Nuclear medicine
topic_unstemmed	misc R895-920 misc radiation misc melatonin misc heart misc nadph oxidase 2 misc nadph oxidase 4 misc Medical physics. Medical radiology. Nuclear medicine
topic_browse	misc R895-920 misc radiation misc melatonin misc heart misc nadph oxidase 2 misc nadph oxidase 4 misc Medical physics. Medical radiology. Nuclear medicine
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title	Modulation of Radiation-Induced NADPH Oxidases in Rat’s Heart Tissues by Melatonin
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title_full	Modulation of Radiation-Induced NADPH Oxidases in Rat’s Heart Tissues by Melatonin
author_sort	Tayebeh Aryafar
journal	Journal of Biomedical Physics and Engineering
journalStr	Journal of Biomedical Physics and Engineering
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author_browse	Tayebeh Aryafar Peyman Amini Saeed Rezapoor Dheyauldeen Shabeeb Ahmed Eleojo Musa Masoud Najafi Alireza Shirazi
container_volume	11
class	R895-920
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author-letter	Tayebeh Aryafar
doi_str_mv	10.31661/jbpe.v0i0.1094
author2-role	verfasserin
title_sort	modulation of radiation-induced nadph oxidases in rat’s heart tissues by melatonin
callnumber	R895-920
title_auth	Modulation of Radiation-Induced NADPH Oxidases in Rat’s Heart Tissues by Melatonin
abstract	Background: Experimental studies have shown that infiltration of inflammatory cells as well as upregulation of some cytokines play a central role in the development of late effects of ionizing radiation in heart tissues. Evidences have shown that an increased level of TGF-β has a direct correlation with late effects of exposure to ionizing radiation such as chronic oxidative stress and fibrosis. Recent studies have shown that TGF-β, through upregulation of pro-oxidant enzymes such as NOX2 and NOX4, promotes continuous ROS production and accumulation of fibrosis. Objective: In present study, we aimed to evaluate the expression of NOX2 and NOX4 signaling pathways as well as possible modulatory effects of melatonin on the expression of these genes.Material and Methods: In this experimental study, four groups of 20 rats (5 in each) were used as follows; G1: control; G2: melatonin; G3: radiation; G4: radiation + melatonin. 100 mg/kg of melatonin was administrated before irradiation of heart tissues with 15 Gy gamma rays. 10 weeks after irradiation, heart tissues were collected for real-time PCR. Results: Results showed a significant increase in the expression of TGF-β, Smad2, NF-kB, NOX2 and NOX4. The upregulation of NOX2 was more obvious by 20-fold compared to other genes. Except for TGF-β, melatonin could attenuate the expression of other genes. Conclusion: This study indicated that exposure of rat’s heart tissues to radiation leads to upregulation of TGF-β-NOX4 and TGF-β-NOX2 pathways. Melatonin, through modulation of these genes, may be able to alleviate radiation-induced chronic oxidative stress and subsequent consequences.
abstractGer	Background: Experimental studies have shown that infiltration of inflammatory cells as well as upregulation of some cytokines play a central role in the development of late effects of ionizing radiation in heart tissues. Evidences have shown that an increased level of TGF-β has a direct correlation with late effects of exposure to ionizing radiation such as chronic oxidative stress and fibrosis. Recent studies have shown that TGF-β, through upregulation of pro-oxidant enzymes such as NOX2 and NOX4, promotes continuous ROS production and accumulation of fibrosis. Objective: In present study, we aimed to evaluate the expression of NOX2 and NOX4 signaling pathways as well as possible modulatory effects of melatonin on the expression of these genes.Material and Methods: In this experimental study, four groups of 20 rats (5 in each) were used as follows; G1: control; G2: melatonin; G3: radiation; G4: radiation + melatonin. 100 mg/kg of melatonin was administrated before irradiation of heart tissues with 15 Gy gamma rays. 10 weeks after irradiation, heart tissues were collected for real-time PCR. Results: Results showed a significant increase in the expression of TGF-β, Smad2, NF-kB, NOX2 and NOX4. The upregulation of NOX2 was more obvious by 20-fold compared to other genes. Except for TGF-β, melatonin could attenuate the expression of other genes. Conclusion: This study indicated that exposure of rat’s heart tissues to radiation leads to upregulation of TGF-β-NOX4 and TGF-β-NOX2 pathways. Melatonin, through modulation of these genes, may be able to alleviate radiation-induced chronic oxidative stress and subsequent consequences.
abstract_unstemmed	Background: Experimental studies have shown that infiltration of inflammatory cells as well as upregulation of some cytokines play a central role in the development of late effects of ionizing radiation in heart tissues. Evidences have shown that an increased level of TGF-β has a direct correlation with late effects of exposure to ionizing radiation such as chronic oxidative stress and fibrosis. Recent studies have shown that TGF-β, through upregulation of pro-oxidant enzymes such as NOX2 and NOX4, promotes continuous ROS production and accumulation of fibrosis. Objective: In present study, we aimed to evaluate the expression of NOX2 and NOX4 signaling pathways as well as possible modulatory effects of melatonin on the expression of these genes.Material and Methods: In this experimental study, four groups of 20 rats (5 in each) were used as follows; G1: control; G2: melatonin; G3: radiation; G4: radiation + melatonin. 100 mg/kg of melatonin was administrated before irradiation of heart tissues with 15 Gy gamma rays. 10 weeks after irradiation, heart tissues were collected for real-time PCR. Results: Results showed a significant increase in the expression of TGF-β, Smad2, NF-kB, NOX2 and NOX4. The upregulation of NOX2 was more obvious by 20-fold compared to other genes. Except for TGF-β, melatonin could attenuate the expression of other genes. Conclusion: This study indicated that exposure of rat’s heart tissues to radiation leads to upregulation of TGF-β-NOX4 and TGF-β-NOX2 pathways. Melatonin, through modulation of these genes, may be able to alleviate radiation-induced chronic oxidative stress and subsequent consequences.
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title_short	Modulation of Radiation-Induced NADPH Oxidases in Rat’s Heart Tissues by Melatonin
url	https://doi.org/10.31661/jbpe.v0i0.1094 https://doaj.org/article/3f5217c4c38a419591d1bb5f5aa6f691 https://jbpe.sums.ac.ir/article_46520_bf6bec5a2a33153f054d9bfeea4e423d.pdf https://doaj.org/toc/2251-7200
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author2	Peyman Amini Saeed Rezapoor Dheyauldeen Shabeeb Ahmed Eleojo Musa Masoud Najafi Alireza Shirazi
author2Str	Peyman Amini Saeed Rezapoor Dheyauldeen Shabeeb Ahmed Eleojo Musa Masoud Najafi Alireza Shirazi
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up_date	2024-07-04T01:19:22.226Z
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