Agomelatine prevents gentamicin nephrotoxicity by attenuating oxidative stress and TLR-4 signaling, and upregulating PPARγ and SIRT1

Kidney injury is a relatively common complication of the use of aminoglycosides. Inflammation and oxidative stress play a key role in gentamicin (GM) nephrotoxicity. We investigated the protective effect of the melatonergic agonist agomelatine (AGM) on GM nephrotoxicity, emphasizing the involvement...
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Gespeichert in:

Autor*in:	Mahmoud, Ayman M. [verfasserIn] Abd El-Ghafar, Omnia A.M. [verfasserIn] Alzoghaibi, Mohammed A. [verfasserIn] Hassanein, Emad H.M. [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	Aminoglycosides Oxidative stress Antidepressant Inflammation TLR-4 Kidney injury

Übergeordnetes Werk:	Enthalten in: Life sciences - New York, NY [u.a.] : Elsevier Science, 1963, 278
Übergeordnetes Werk:	volume:278

DOI / URN:	10.1016/j.lfs.2021.119600

Katalog-ID:	ELV006167055

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520			\|a Kidney injury is a relatively common complication of the use of aminoglycosides. Inflammation and oxidative stress play a key role in gentamicin (GM) nephrotoxicity. We investigated the protective effect of the melatonergic agonist agomelatine (AGM) on GM nephrotoxicity, emphasizing the involvement of TLR-4 signaling, SIRT1 and PPARγ. Rats received 25 mg/kg AGM for 15 days and 100 mg/kg GM for eight days starting at day 7. Elevated serum creatinine, urea and Kim-1 along with multiple histological alterations in the kidney were observed in GM-intoxicated rats. Malondialdehyde (MDA), TNF-α, IL-1β, nitric oxide (NO) and myeloperoxidase (MPO) were increased, and GSH, SOD and catalase were decreased in the kidney of GM-intoxicated rats. Treatment with AGM significantly ameliorated the kidney function biomarkers, prevented tissue injury, decreased inflammatory cytokines, MDA, NO and MPO, and boosted antioxidants. In addition, AGM suppressed the expression of TLR-4, NF-κB p65, p38 MAPK, ERK-1, VCAM-1 and iNOS, whereas upregulated SIRT1 and PPARγ in the kidney of GM-intoxicated rats. In conclusion, AGM prevented GM nephrotoxicity in rats by attenuating oxidative injury and inflammation. AGM suppressed TLR-4 signaling, enhanced antioxidants and upregulated SIRT1 and PPARγ in the kidney of GM-induced rats.
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author_variant	a m m am amm e g o a a egoa egoaa m a a ma maa e h h eh ehh
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allfields	10.1016/j.lfs.2021.119600 doi (DE-627)ELV006167055 (ELSEVIER)S0024-3205(21)00586-5 DE-627 ger DE-627 rda eng 570 DE-600 BIODIV DE-30 fid 42.00 bkl 44.40 bkl Mahmoud, Ayman M. verfasserin aut Agomelatine prevents gentamicin nephrotoxicity by attenuating oxidative stress and TLR-4 signaling, and upregulating PPARγ and SIRT1 2021 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Kidney injury is a relatively common complication of the use of aminoglycosides. Inflammation and oxidative stress play a key role in gentamicin (GM) nephrotoxicity. We investigated the protective effect of the melatonergic agonist agomelatine (AGM) on GM nephrotoxicity, emphasizing the involvement of TLR-4 signaling, SIRT1 and PPARγ. Rats received 25 mg/kg AGM for 15 days and 100 mg/kg GM for eight days starting at day 7. Elevated serum creatinine, urea and Kim-1 along with multiple histological alterations in the kidney were observed in GM-intoxicated rats. Malondialdehyde (MDA), TNF-α, IL-1β, nitric oxide (NO) and myeloperoxidase (MPO) were increased, and GSH, SOD and catalase were decreased in the kidney of GM-intoxicated rats. Treatment with AGM significantly ameliorated the kidney function biomarkers, prevented tissue injury, decreased inflammatory cytokines, MDA, NO and MPO, and boosted antioxidants. In addition, AGM suppressed the expression of TLR-4, NF-κB p65, p38 MAPK, ERK-1, VCAM-1 and iNOS, whereas upregulated SIRT1 and PPARγ in the kidney of GM-intoxicated rats. In conclusion, AGM prevented GM nephrotoxicity in rats by attenuating oxidative injury and inflammation. AGM suppressed TLR-4 signaling, enhanced antioxidants and upregulated SIRT1 and PPARγ in the kidney of GM-induced rats. Aminoglycosides Oxidative stress Antidepressant Inflammation TLR-4 Kidney injury Abd El-Ghafar, Omnia A.M. verfasserin aut Alzoghaibi, Mohammed A. verfasserin aut Hassanein, Emad H.M. verfasserin aut Enthalten in Life sciences New York, NY [u.a.] : Elsevier Science, 1963 278 Online-Ressource (DE-627)320515605 (DE-600)2013911-1 (DE-576)09095503X 1879-0631 nnns volume:278 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-BIODIV SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2336 GBV_ILN_4037 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4313 GBV_ILN_4326 GBV_ILN_4334 GBV_ILN_4338 42.00 Biologie: Allgemeines 44.40 Pharmazie Pharmazeutika AR 278
spelling	10.1016/j.lfs.2021.119600 doi (DE-627)ELV006167055 (ELSEVIER)S0024-3205(21)00586-5 DE-627 ger DE-627 rda eng 570 DE-600 BIODIV DE-30 fid 42.00 bkl 44.40 bkl Mahmoud, Ayman M. verfasserin aut Agomelatine prevents gentamicin nephrotoxicity by attenuating oxidative stress and TLR-4 signaling, and upregulating PPARγ and SIRT1 2021 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Kidney injury is a relatively common complication of the use of aminoglycosides. Inflammation and oxidative stress play a key role in gentamicin (GM) nephrotoxicity. We investigated the protective effect of the melatonergic agonist agomelatine (AGM) on GM nephrotoxicity, emphasizing the involvement of TLR-4 signaling, SIRT1 and PPARγ. Rats received 25 mg/kg AGM for 15 days and 100 mg/kg GM for eight days starting at day 7. Elevated serum creatinine, urea and Kim-1 along with multiple histological alterations in the kidney were observed in GM-intoxicated rats. Malondialdehyde (MDA), TNF-α, IL-1β, nitric oxide (NO) and myeloperoxidase (MPO) were increased, and GSH, SOD and catalase were decreased in the kidney of GM-intoxicated rats. Treatment with AGM significantly ameliorated the kidney function biomarkers, prevented tissue injury, decreased inflammatory cytokines, MDA, NO and MPO, and boosted antioxidants. In addition, AGM suppressed the expression of TLR-4, NF-κB p65, p38 MAPK, ERK-1, VCAM-1 and iNOS, whereas upregulated SIRT1 and PPARγ in the kidney of GM-intoxicated rats. In conclusion, AGM prevented GM nephrotoxicity in rats by attenuating oxidative injury and inflammation. AGM suppressed TLR-4 signaling, enhanced antioxidants and upregulated SIRT1 and PPARγ in the kidney of GM-induced rats. Aminoglycosides Oxidative stress Antidepressant Inflammation TLR-4 Kidney injury Abd El-Ghafar, Omnia A.M. verfasserin aut Alzoghaibi, Mohammed A. verfasserin aut Hassanein, Emad H.M. verfasserin aut Enthalten in Life sciences New York, NY [u.a.] : Elsevier Science, 1963 278 Online-Ressource (DE-627)320515605 (DE-600)2013911-1 (DE-576)09095503X 1879-0631 nnns volume:278 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-BIODIV SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2336 GBV_ILN_4037 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4313 GBV_ILN_4326 GBV_ILN_4334 GBV_ILN_4338 42.00 Biologie: Allgemeines 44.40 Pharmazie Pharmazeutika AR 278
allfields_unstemmed	10.1016/j.lfs.2021.119600 doi (DE-627)ELV006167055 (ELSEVIER)S0024-3205(21)00586-5 DE-627 ger DE-627 rda eng 570 DE-600 BIODIV DE-30 fid 42.00 bkl 44.40 bkl Mahmoud, Ayman M. verfasserin aut Agomelatine prevents gentamicin nephrotoxicity by attenuating oxidative stress and TLR-4 signaling, and upregulating PPARγ and SIRT1 2021 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Kidney injury is a relatively common complication of the use of aminoglycosides. Inflammation and oxidative stress play a key role in gentamicin (GM) nephrotoxicity. We investigated the protective effect of the melatonergic agonist agomelatine (AGM) on GM nephrotoxicity, emphasizing the involvement of TLR-4 signaling, SIRT1 and PPARγ. Rats received 25 mg/kg AGM for 15 days and 100 mg/kg GM for eight days starting at day 7. Elevated serum creatinine, urea and Kim-1 along with multiple histological alterations in the kidney were observed in GM-intoxicated rats. Malondialdehyde (MDA), TNF-α, IL-1β, nitric oxide (NO) and myeloperoxidase (MPO) were increased, and GSH, SOD and catalase were decreased in the kidney of GM-intoxicated rats. Treatment with AGM significantly ameliorated the kidney function biomarkers, prevented tissue injury, decreased inflammatory cytokines, MDA, NO and MPO, and boosted antioxidants. In addition, AGM suppressed the expression of TLR-4, NF-κB p65, p38 MAPK, ERK-1, VCAM-1 and iNOS, whereas upregulated SIRT1 and PPARγ in the kidney of GM-intoxicated rats. In conclusion, AGM prevented GM nephrotoxicity in rats by attenuating oxidative injury and inflammation. AGM suppressed TLR-4 signaling, enhanced antioxidants and upregulated SIRT1 and PPARγ in the kidney of GM-induced rats. Aminoglycosides Oxidative stress Antidepressant Inflammation TLR-4 Kidney injury Abd El-Ghafar, Omnia A.M. verfasserin aut Alzoghaibi, Mohammed A. verfasserin aut Hassanein, Emad H.M. verfasserin aut Enthalten in Life sciences New York, NY [u.a.] : Elsevier Science, 1963 278 Online-Ressource (DE-627)320515605 (DE-600)2013911-1 (DE-576)09095503X 1879-0631 nnns volume:278 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-BIODIV SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2336 GBV_ILN_4037 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4313 GBV_ILN_4326 GBV_ILN_4334 GBV_ILN_4338 42.00 Biologie: Allgemeines 44.40 Pharmazie Pharmazeutika AR 278
allfieldsGer	10.1016/j.lfs.2021.119600 doi (DE-627)ELV006167055 (ELSEVIER)S0024-3205(21)00586-5 DE-627 ger DE-627 rda eng 570 DE-600 BIODIV DE-30 fid 42.00 bkl 44.40 bkl Mahmoud, Ayman M. verfasserin aut Agomelatine prevents gentamicin nephrotoxicity by attenuating oxidative stress and TLR-4 signaling, and upregulating PPARγ and SIRT1 2021 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Kidney injury is a relatively common complication of the use of aminoglycosides. Inflammation and oxidative stress play a key role in gentamicin (GM) nephrotoxicity. We investigated the protective effect of the melatonergic agonist agomelatine (AGM) on GM nephrotoxicity, emphasizing the involvement of TLR-4 signaling, SIRT1 and PPARγ. Rats received 25 mg/kg AGM for 15 days and 100 mg/kg GM for eight days starting at day 7. Elevated serum creatinine, urea and Kim-1 along with multiple histological alterations in the kidney were observed in GM-intoxicated rats. Malondialdehyde (MDA), TNF-α, IL-1β, nitric oxide (NO) and myeloperoxidase (MPO) were increased, and GSH, SOD and catalase were decreased in the kidney of GM-intoxicated rats. Treatment with AGM significantly ameliorated the kidney function biomarkers, prevented tissue injury, decreased inflammatory cytokines, MDA, NO and MPO, and boosted antioxidants. In addition, AGM suppressed the expression of TLR-4, NF-κB p65, p38 MAPK, ERK-1, VCAM-1 and iNOS, whereas upregulated SIRT1 and PPARγ in the kidney of GM-intoxicated rats. In conclusion, AGM prevented GM nephrotoxicity in rats by attenuating oxidative injury and inflammation. AGM suppressed TLR-4 signaling, enhanced antioxidants and upregulated SIRT1 and PPARγ in the kidney of GM-induced rats. Aminoglycosides Oxidative stress Antidepressant Inflammation TLR-4 Kidney injury Abd El-Ghafar, Omnia A.M. verfasserin aut Alzoghaibi, Mohammed A. verfasserin aut Hassanein, Emad H.M. verfasserin aut Enthalten in Life sciences New York, NY [u.a.] : Elsevier Science, 1963 278 Online-Ressource (DE-627)320515605 (DE-600)2013911-1 (DE-576)09095503X 1879-0631 nnns volume:278 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-BIODIV SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2336 GBV_ILN_4037 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4313 GBV_ILN_4326 GBV_ILN_4334 GBV_ILN_4338 42.00 Biologie: Allgemeines 44.40 Pharmazie Pharmazeutika AR 278
allfieldsSound	10.1016/j.lfs.2021.119600 doi (DE-627)ELV006167055 (ELSEVIER)S0024-3205(21)00586-5 DE-627 ger DE-627 rda eng 570 DE-600 BIODIV DE-30 fid 42.00 bkl 44.40 bkl Mahmoud, Ayman M. verfasserin aut Agomelatine prevents gentamicin nephrotoxicity by attenuating oxidative stress and TLR-4 signaling, and upregulating PPARγ and SIRT1 2021 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Kidney injury is a relatively common complication of the use of aminoglycosides. Inflammation and oxidative stress play a key role in gentamicin (GM) nephrotoxicity. We investigated the protective effect of the melatonergic agonist agomelatine (AGM) on GM nephrotoxicity, emphasizing the involvement of TLR-4 signaling, SIRT1 and PPARγ. Rats received 25 mg/kg AGM for 15 days and 100 mg/kg GM for eight days starting at day 7. Elevated serum creatinine, urea and Kim-1 along with multiple histological alterations in the kidney were observed in GM-intoxicated rats. Malondialdehyde (MDA), TNF-α, IL-1β, nitric oxide (NO) and myeloperoxidase (MPO) were increased, and GSH, SOD and catalase were decreased in the kidney of GM-intoxicated rats. Treatment with AGM significantly ameliorated the kidney function biomarkers, prevented tissue injury, decreased inflammatory cytokines, MDA, NO and MPO, and boosted antioxidants. In addition, AGM suppressed the expression of TLR-4, NF-κB p65, p38 MAPK, ERK-1, VCAM-1 and iNOS, whereas upregulated SIRT1 and PPARγ in the kidney of GM-intoxicated rats. In conclusion, AGM prevented GM nephrotoxicity in rats by attenuating oxidative injury and inflammation. AGM suppressed TLR-4 signaling, enhanced antioxidants and upregulated SIRT1 and PPARγ in the kidney of GM-induced rats. Aminoglycosides Oxidative stress Antidepressant Inflammation TLR-4 Kidney injury Abd El-Ghafar, Omnia A.M. verfasserin aut Alzoghaibi, Mohammed A. verfasserin aut Hassanein, Emad H.M. verfasserin aut Enthalten in Life sciences New York, NY [u.a.] : Elsevier Science, 1963 278 Online-Ressource (DE-627)320515605 (DE-600)2013911-1 (DE-576)09095503X 1879-0631 nnns volume:278 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-BIODIV SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2336 GBV_ILN_4037 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4313 GBV_ILN_4326 GBV_ILN_4334 GBV_ILN_4338 42.00 Biologie: Allgemeines 44.40 Pharmazie Pharmazeutika AR 278
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topic_facet	Aminoglycosides Oxidative stress Antidepressant Inflammation TLR-4 Kidney injury
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authorswithroles_txt_mv	Mahmoud, Ayman M. @@aut@@ Abd El-Ghafar, Omnia A.M. @@aut@@ Alzoghaibi, Mohammed A. @@aut@@ Hassanein, Emad H.M. @@aut@@
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author	Mahmoud, Ayman M.
spellingShingle	Mahmoud, Ayman M. ddc 570 fid BIODIV bkl 42.00 bkl 44.40 misc Aminoglycosides misc Oxidative stress misc Antidepressant misc Inflammation misc TLR-4 misc Kidney injury Agomelatine prevents gentamicin nephrotoxicity by attenuating oxidative stress and TLR-4 signaling, and upregulating PPARγ and SIRT1
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topic_title	570 DE-600 BIODIV DE-30 fid 42.00 bkl 44.40 bkl Agomelatine prevents gentamicin nephrotoxicity by attenuating oxidative stress and TLR-4 signaling, and upregulating PPARγ and SIRT1 Aminoglycosides Oxidative stress Antidepressant Inflammation TLR-4 Kidney injury
topic	ddc 570 fid BIODIV bkl 42.00 bkl 44.40 misc Aminoglycosides misc Oxidative stress misc Antidepressant misc Inflammation misc TLR-4 misc Kidney injury
topic_unstemmed	ddc 570 fid BIODIV bkl 42.00 bkl 44.40 misc Aminoglycosides misc Oxidative stress misc Antidepressant misc Inflammation misc TLR-4 misc Kidney injury
topic_browse	ddc 570 fid BIODIV bkl 42.00 bkl 44.40 misc Aminoglycosides misc Oxidative stress misc Antidepressant misc Inflammation misc TLR-4 misc Kidney injury
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title	Agomelatine prevents gentamicin nephrotoxicity by attenuating oxidative stress and TLR-4 signaling, and upregulating PPARγ and SIRT1
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title_full	Agomelatine prevents gentamicin nephrotoxicity by attenuating oxidative stress and TLR-4 signaling, and upregulating PPARγ and SIRT1
author_sort	Mahmoud, Ayman M.
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author_browse	Mahmoud, Ayman M. Abd El-Ghafar, Omnia A.M. Alzoghaibi, Mohammed A. Hassanein, Emad H.M.
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author-letter	Mahmoud, Ayman M.
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title_sort	agomelatine prevents gentamicin nephrotoxicity by attenuating oxidative stress and tlr-4 signaling, and upregulating pparγ and sirt1
title_auth	Agomelatine prevents gentamicin nephrotoxicity by attenuating oxidative stress and TLR-4 signaling, and upregulating PPARγ and SIRT1
abstract	Kidney injury is a relatively common complication of the use of aminoglycosides. Inflammation and oxidative stress play a key role in gentamicin (GM) nephrotoxicity. We investigated the protective effect of the melatonergic agonist agomelatine (AGM) on GM nephrotoxicity, emphasizing the involvement of TLR-4 signaling, SIRT1 and PPARγ. Rats received 25 mg/kg AGM for 15 days and 100 mg/kg GM for eight days starting at day 7. Elevated serum creatinine, urea and Kim-1 along with multiple histological alterations in the kidney were observed in GM-intoxicated rats. Malondialdehyde (MDA), TNF-α, IL-1β, nitric oxide (NO) and myeloperoxidase (MPO) were increased, and GSH, SOD and catalase were decreased in the kidney of GM-intoxicated rats. Treatment with AGM significantly ameliorated the kidney function biomarkers, prevented tissue injury, decreased inflammatory cytokines, MDA, NO and MPO, and boosted antioxidants. In addition, AGM suppressed the expression of TLR-4, NF-κB p65, p38 MAPK, ERK-1, VCAM-1 and iNOS, whereas upregulated SIRT1 and PPARγ in the kidney of GM-intoxicated rats. In conclusion, AGM prevented GM nephrotoxicity in rats by attenuating oxidative injury and inflammation. AGM suppressed TLR-4 signaling, enhanced antioxidants and upregulated SIRT1 and PPARγ in the kidney of GM-induced rats.
abstractGer	Kidney injury is a relatively common complication of the use of aminoglycosides. Inflammation and oxidative stress play a key role in gentamicin (GM) nephrotoxicity. We investigated the protective effect of the melatonergic agonist agomelatine (AGM) on GM nephrotoxicity, emphasizing the involvement of TLR-4 signaling, SIRT1 and PPARγ. Rats received 25 mg/kg AGM for 15 days and 100 mg/kg GM for eight days starting at day 7. Elevated serum creatinine, urea and Kim-1 along with multiple histological alterations in the kidney were observed in GM-intoxicated rats. Malondialdehyde (MDA), TNF-α, IL-1β, nitric oxide (NO) and myeloperoxidase (MPO) were increased, and GSH, SOD and catalase were decreased in the kidney of GM-intoxicated rats. Treatment with AGM significantly ameliorated the kidney function biomarkers, prevented tissue injury, decreased inflammatory cytokines, MDA, NO and MPO, and boosted antioxidants. In addition, AGM suppressed the expression of TLR-4, NF-κB p65, p38 MAPK, ERK-1, VCAM-1 and iNOS, whereas upregulated SIRT1 and PPARγ in the kidney of GM-intoxicated rats. In conclusion, AGM prevented GM nephrotoxicity in rats by attenuating oxidative injury and inflammation. AGM suppressed TLR-4 signaling, enhanced antioxidants and upregulated SIRT1 and PPARγ in the kidney of GM-induced rats.
abstract_unstemmed	Kidney injury is a relatively common complication of the use of aminoglycosides. Inflammation and oxidative stress play a key role in gentamicin (GM) nephrotoxicity. We investigated the protective effect of the melatonergic agonist agomelatine (AGM) on GM nephrotoxicity, emphasizing the involvement of TLR-4 signaling, SIRT1 and PPARγ. Rats received 25 mg/kg AGM for 15 days and 100 mg/kg GM for eight days starting at day 7. Elevated serum creatinine, urea and Kim-1 along with multiple histological alterations in the kidney were observed in GM-intoxicated rats. Malondialdehyde (MDA), TNF-α, IL-1β, nitric oxide (NO) and myeloperoxidase (MPO) were increased, and GSH, SOD and catalase were decreased in the kidney of GM-intoxicated rats. Treatment with AGM significantly ameliorated the kidney function biomarkers, prevented tissue injury, decreased inflammatory cytokines, MDA, NO and MPO, and boosted antioxidants. In addition, AGM suppressed the expression of TLR-4, NF-κB p65, p38 MAPK, ERK-1, VCAM-1 and iNOS, whereas upregulated SIRT1 and PPARγ in the kidney of GM-intoxicated rats. In conclusion, AGM prevented GM nephrotoxicity in rats by attenuating oxidative injury and inflammation. AGM suppressed TLR-4 signaling, enhanced antioxidants and upregulated SIRT1 and PPARγ in the kidney of GM-induced rats.
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title_short	Agomelatine prevents gentamicin nephrotoxicity by attenuating oxidative stress and TLR-4 signaling, and upregulating PPARγ and SIRT1
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author2	Abd El-Ghafar, Omnia A.M. Alzoghaibi, Mohammed A. Hassanein, Emad H.M.
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up_date	2024-07-06T20:27:09.331Z
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In addition, AGM suppressed the expression of TLR-4, NF-κB p65, p38 MAPK, ERK-1, VCAM-1 and iNOS, whereas upregulated SIRT1 and PPARγ in the kidney of GM-intoxicated rats. In conclusion, AGM prevented GM nephrotoxicity in rats by attenuating oxidative injury and inflammation. 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Agomelatine prevents gentamicin nephrotoxicity by attenuating oxidative stress and TLR-4 signaling, and upregulating PPARγ and SIRT1

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