Apremilast prevent doxorubicin-induced apoptosis and inflammation in heart through inhibition of oxidative stress mediated activation of NF-κB signaling pathways
Copyright © 2018 Institute of Pharmacology, Polish Academy of Sciences. Published by Elsevier B.V. All rights reserved..
BACKGROUND: Doxorubicin is an effective, potent and commonly used anthracycline-related anticancer drug; however, cardiotoxicity compromises its therapeutic potential. Apremilast, a novel phosphodiesterase type 4-inhibitor, reported to have anti-inflammatory effects and modulating many inflammatory mediators.
METHODS: The present study investigated the influence of apremilast against doxorubicin-induced cardiotoxicity in male Wistar rats. A total, 24 animals were divided into four groups of six animal each. Group 1, served as control and received normal saline. Group 2 animals, received doxorubicin (20mgkg-1, ip). Group 3 and 4, treatment group, received doxorubicin (20mgkg-1, ip) with the same schedule as group-2, plus apremilast (10 and 20mgkg-1day-1, po) respectively. Oxidative stress, caspase-3 enzyme activity, gene expression and protein expression were tested.
RESULTS: The results of the present study demonstrated that administration of apremilast reversed doxorubicin-induced cardiotoxicity.
CONCLUSION: These findings suggested that apremilast can attenuate doxorubicin-induced cardiotoxicity via inhibition of oxidative stress mediated activation of nuclear factor-kappa B signaling pathways.
Errataetall: |
ErratumIn: Pharmacol Rep. 2019 Dec;71(6):1227. - PMID 31669887 |
---|---|
Medienart: |
E-Artikel |
Erscheinungsjahr: |
2018 |
---|---|
Erschienen: |
2018 |
Enthalten in: |
Zur Gesamtaufnahme - volume:70 |
---|---|
Enthalten in: |
Pharmacological reports : PR - 70(2018), 5 vom: 01. Okt., Seite 993-1000 |
Sprache: |
Englisch |
---|
Beteiligte Personen: |
Imam, Faisal [VerfasserIn] |
---|
Links: |
---|
Anmerkungen: |
Date Completed 16.11.2018 Date Revised 06.01.2020 published: Print-Electronic ErratumIn: Pharmacol Rep. 2019 Dec;71(6):1227. - PMID 31669887 Citation Status MEDLINE |
---|
doi: |
10.1016/j.pharep.2018.03.009 |
---|
funding: |
|
---|---|
Förderinstitution / Projekttitel: |
|
PPN (Katalog-ID): |
NLM287576892 |
---|
LEADER | 01000naa a22002652 4500 | ||
---|---|---|---|
001 | NLM287576892 | ||
003 | DE-627 | ||
005 | 20231225054326.0 | ||
007 | cr uuu---uuuuu | ||
008 | 231225s2018 xx |||||o 00| ||eng c | ||
024 | 7 | |a 10.1016/j.pharep.2018.03.009 |2 doi | |
028 | 5 | 2 | |a pubmed24n0958.xml |
035 | |a (DE-627)NLM287576892 | ||
035 | |a (NLM)30118964 | ||
035 | |a (PII)S1734-1140(17)30667-9 | ||
040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
041 | |a eng | ||
100 | 1 | |a Imam, Faisal |e verfasserin |4 aut | |
245 | 1 | 0 | |a Apremilast prevent doxorubicin-induced apoptosis and inflammation in heart through inhibition of oxidative stress mediated activation of NF-κB signaling pathways |
264 | 1 | |c 2018 | |
336 | |a Text |b txt |2 rdacontent | ||
337 | |a ƒaComputermedien |b c |2 rdamedia | ||
338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
500 | |a Date Completed 16.11.2018 | ||
500 | |a Date Revised 06.01.2020 | ||
500 | |a published: Print-Electronic | ||
500 | |a ErratumIn: Pharmacol Rep. 2019 Dec;71(6):1227. - PMID 31669887 | ||
500 | |a Citation Status MEDLINE | ||
520 | |a Copyright © 2018 Institute of Pharmacology, Polish Academy of Sciences. Published by Elsevier B.V. All rights reserved. | ||
520 | |a BACKGROUND: Doxorubicin is an effective, potent and commonly used anthracycline-related anticancer drug; however, cardiotoxicity compromises its therapeutic potential. Apremilast, a novel phosphodiesterase type 4-inhibitor, reported to have anti-inflammatory effects and modulating many inflammatory mediators | ||
520 | |a METHODS: The present study investigated the influence of apremilast against doxorubicin-induced cardiotoxicity in male Wistar rats. A total, 24 animals were divided into four groups of six animal each. Group 1, served as control and received normal saline. Group 2 animals, received doxorubicin (20mgkg-1, ip). Group 3 and 4, treatment group, received doxorubicin (20mgkg-1, ip) with the same schedule as group-2, plus apremilast (10 and 20mgkg-1day-1, po) respectively. Oxidative stress, caspase-3 enzyme activity, gene expression and protein expression were tested | ||
520 | |a RESULTS: The results of the present study demonstrated that administration of apremilast reversed doxorubicin-induced cardiotoxicity | ||
520 | |a CONCLUSION: These findings suggested that apremilast can attenuate doxorubicin-induced cardiotoxicity via inhibition of oxidative stress mediated activation of nuclear factor-kappa B signaling pathways | ||
650 | 4 | |a Journal Article | |
650 | 4 | |a Apremilast | |
650 | 4 | |a Cardiotoxicity | |
650 | 4 | |a Doxorubicin | |
650 | 4 | |a Inflammation | |
650 | 4 | |a Nuclear factor-kappa B | |
650 | 7 | |a NF-kappa B |2 NLM | |
650 | 7 | |a RNA, Messenger |2 NLM | |
650 | 7 | |a Malondialdehyde |2 NLM | |
650 | 7 | |a 4Y8F71G49Q |2 NLM | |
650 | 7 | |a Thalidomide |2 NLM | |
650 | 7 | |a 4Z8R6ORS6L |2 NLM | |
650 | 7 | |a Doxorubicin |2 NLM | |
650 | 7 | |a 80168379AG |2 NLM | |
650 | 7 | |a Catalase |2 NLM | |
650 | 7 | |a EC 1.11.1.6 |2 NLM | |
650 | 7 | |a Glutathione Reductase |2 NLM | |
650 | 7 | |a EC 1.8.1.7 |2 NLM | |
650 | 7 | |a Caspase 3 |2 NLM | |
650 | 7 | |a EC 3.4.22.- |2 NLM | |
650 | 7 | |a Glutathione |2 NLM | |
650 | 7 | |a GAN16C9B8O |2 NLM | |
650 | 7 | |a apremilast |2 NLM | |
650 | 7 | |a UP7QBP99PN |2 NLM | |
700 | 1 | |a Al-Harbi, Naif O |e verfasserin |4 aut | |
700 | 1 | |a Al-Harbi, Mohammad Matar |e verfasserin |4 aut | |
700 | 1 | |a Ansari, Mushtaq Ahmad |e verfasserin |4 aut | |
700 | 1 | |a Al-Asmari, Abdullah F |e verfasserin |4 aut | |
700 | 1 | |a Ansari, Mohd Nazam |e verfasserin |4 aut | |
700 | 1 | |a Al-Anazi, Wael A |e verfasserin |4 aut | |
700 | 1 | |a Bahashwan, Saleh |e verfasserin |4 aut | |
700 | 1 | |a Almutairi, Mashal M |e verfasserin |4 aut | |
700 | 1 | |a Alshammari, Musaad |e verfasserin |4 aut | |
700 | 1 | |a Khan, Mohammad Rashid |e verfasserin |4 aut | |
700 | 1 | |a Alsaad, Abdulaziz Mohammed |e verfasserin |4 aut | |
700 | 1 | |a Alotaibi, Moureq Rashed |e verfasserin |4 aut | |
773 | 0 | 8 | |i Enthalten in |t Pharmacological reports : PR |d 2005 |g 70(2018), 5 vom: 01. Okt., Seite 993-1000 |w (DE-627)NLM154978965 |x 2299-5684 |7 nnns |
773 | 1 | 8 | |g volume:70 |g year:2018 |g number:5 |g day:01 |g month:10 |g pages:993-1000 |
856 | 4 | 0 | |u http://dx.doi.org/10.1016/j.pharep.2018.03.009 |3 Volltext |
912 | |a GBV_USEFLAG_A | ||
912 | |a GBV_NLM | ||
951 | |a AR | ||
952 | |d 70 |j 2018 |e 5 |b 01 |c 10 |h 993-1000 |