Renoprotective effects of levosimendan on acute kidney injury following cardiac arrest via anti‐inflammation, anti‐apoptosis, and ERK activation

ATP‐sensitive potassium channels (KATPs) have protective effects in ischemia–reperfusion‐induced injuries and can be activated by levosimendan. This study investigated the effects of levosimendan on renal injury, inflammation, apoptosis, and survival in a rat model of acute kidney injury (AKI) follo...
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Autor*in:	Lei Tian [verfasserIn] Shiwei Wang [verfasserIn] Li Zhao [verfasserIn] Xiaoye Lu [verfasserIn] Changqing Zhu [verfasserIn] Hao Gong [verfasserIn] Weiqiang Yang [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	acute kidney injury cardiac arrest cardiopulmonary resuscitation ERK levosimendan

Übergeordnetes Werk:	In: FEBS Open Bio - Wiley, 2013, 11(2021), 8, Seite 2236-2244
Übergeordnetes Werk:	volume:11 ; year:2021 ; number:8 ; pages:2236-2244

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1002/2211-5463.13227

Katalog-ID:	DOAJ070169357

Internformat


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520			\|a ATP‐sensitive potassium channels (KATPs) have protective effects in ischemia–reperfusion‐induced injuries and can be activated by levosimendan. This study investigated the effects of levosimendan on renal injury, inflammation, apoptosis, and survival in a rat model of acute kidney injury (AKI) following cardiac arrest (CA) and cardiopulmonary resuscitation (CPR). Rats underwent a 5‐min asphyxia‐based CA and resuscitation. The rats were treated with levosimendan after successful resuscitation. Renal functions, histological changes, inflammatory responses, and apoptosis were examined. NRK‐52E cells treated by hypoxia/reoxygenation (H/R) were used to establish an in vitro CA‐CPR model. Rats in the CA‐induced AKI group had a low survival rate and increased levels of creatinine, blood urea nitrogen, and proinflammatory cytokines, as well as increased tubular injury. These results were significantly reversed after treatment with levosimendan. Levosimendan downregulated the expression of the apoptosis‐related proteins Bax, cleaved caspase‐3, and cleaved caspase‐9, as well as upregulated Bcl‐2 and p‐ERK expression in vivo and in vitro. Thus, our data suggest that levosimendan reduces mortality and AKI following CA and CPR via suppression of inflammation and apoptosis, and activation of ERK signaling.
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allfieldsGer	10.1002/2211-5463.13227 doi (DE-627)DOAJ070169357 (DE-599)DOAJ432c7339c3a44bcb8837d971d8ec1408 DE-627 ger DE-627 rakwb eng QH301-705.5 Lei Tian verfasserin aut Renoprotective effects of levosimendan on acute kidney injury following cardiac arrest via anti‐inflammation, anti‐apoptosis, and ERK activation 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier ATP‐sensitive potassium channels (KATPs) have protective effects in ischemia–reperfusion‐induced injuries and can be activated by levosimendan. This study investigated the effects of levosimendan on renal injury, inflammation, apoptosis, and survival in a rat model of acute kidney injury (AKI) following cardiac arrest (CA) and cardiopulmonary resuscitation (CPR). Rats underwent a 5‐min asphyxia‐based CA and resuscitation. The rats were treated with levosimendan after successful resuscitation. Renal functions, histological changes, inflammatory responses, and apoptosis were examined. NRK‐52E cells treated by hypoxia/reoxygenation (H/R) were used to establish an in vitro CA‐CPR model. Rats in the CA‐induced AKI group had a low survival rate and increased levels of creatinine, blood urea nitrogen, and proinflammatory cytokines, as well as increased tubular injury. These results were significantly reversed after treatment with levosimendan. Levosimendan downregulated the expression of the apoptosis‐related proteins Bax, cleaved caspase‐3, and cleaved caspase‐9, as well as upregulated Bcl‐2 and p‐ERK expression in vivo and in vitro. Thus, our data suggest that levosimendan reduces mortality and AKI following CA and CPR via suppression of inflammation and apoptosis, and activation of ERK signaling. acute kidney injury cardiac arrest cardiopulmonary resuscitation ERK levosimendan Biology (General) Shiwei Wang verfasserin aut Li Zhao verfasserin aut Xiaoye Lu verfasserin aut Changqing Zhu verfasserin aut Hao Gong verfasserin aut Weiqiang Yang verfasserin aut In FEBS Open Bio Wiley, 2013 11(2021), 8, Seite 2236-2244 (DE-627)686948351 (DE-600)2651702-4 22115463 nnns volume:11 year:2021 number:8 pages:2236-2244 https://doi.org/10.1002/2211-5463.13227 kostenfrei https://doaj.org/article/432c7339c3a44bcb8837d971d8ec1408 kostenfrei https://doi.org/10.1002/2211-5463.13227 kostenfrei https://doaj.org/toc/2211-5463 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_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 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_171 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2021 8 2236-2244
allfieldsSound	10.1002/2211-5463.13227 doi (DE-627)DOAJ070169357 (DE-599)DOAJ432c7339c3a44bcb8837d971d8ec1408 DE-627 ger DE-627 rakwb eng QH301-705.5 Lei Tian verfasserin aut Renoprotective effects of levosimendan on acute kidney injury following cardiac arrest via anti‐inflammation, anti‐apoptosis, and ERK activation 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier ATP‐sensitive potassium channels (KATPs) have protective effects in ischemia–reperfusion‐induced injuries and can be activated by levosimendan. This study investigated the effects of levosimendan on renal injury, inflammation, apoptosis, and survival in a rat model of acute kidney injury (AKI) following cardiac arrest (CA) and cardiopulmonary resuscitation (CPR). Rats underwent a 5‐min asphyxia‐based CA and resuscitation. The rats were treated with levosimendan after successful resuscitation. Renal functions, histological changes, inflammatory responses, and apoptosis were examined. NRK‐52E cells treated by hypoxia/reoxygenation (H/R) were used to establish an in vitro CA‐CPR model. Rats in the CA‐induced AKI group had a low survival rate and increased levels of creatinine, blood urea nitrogen, and proinflammatory cytokines, as well as increased tubular injury. These results were significantly reversed after treatment with levosimendan. Levosimendan downregulated the expression of the apoptosis‐related proteins Bax, cleaved caspase‐3, and cleaved caspase‐9, as well as upregulated Bcl‐2 and p‐ERK expression in vivo and in vitro. Thus, our data suggest that levosimendan reduces mortality and AKI following CA and CPR via suppression of inflammation and apoptosis, and activation of ERK signaling. acute kidney injury cardiac arrest cardiopulmonary resuscitation ERK levosimendan Biology (General) Shiwei Wang verfasserin aut Li Zhao verfasserin aut Xiaoye Lu verfasserin aut Changqing Zhu verfasserin aut Hao Gong verfasserin aut Weiqiang Yang verfasserin aut In FEBS Open Bio Wiley, 2013 11(2021), 8, Seite 2236-2244 (DE-627)686948351 (DE-600)2651702-4 22115463 nnns volume:11 year:2021 number:8 pages:2236-2244 https://doi.org/10.1002/2211-5463.13227 kostenfrei https://doaj.org/article/432c7339c3a44bcb8837d971d8ec1408 kostenfrei https://doi.org/10.1002/2211-5463.13227 kostenfrei https://doaj.org/toc/2211-5463 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_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 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_171 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2021 8 2236-2244
language	English
source	In FEBS Open Bio 11(2021), 8, Seite 2236-2244 volume:11 year:2021 number:8 pages:2236-2244
sourceStr	In FEBS Open Bio 11(2021), 8, Seite 2236-2244 volume:11 year:2021 number:8 pages:2236-2244
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	acute kidney injury cardiac arrest cardiopulmonary resuscitation ERK levosimendan Biology (General)
isfreeaccess_bool	true
container_title	FEBS Open Bio
authorswithroles_txt_mv	Lei Tian @@aut@@ Shiwei Wang @@aut@@ Li Zhao @@aut@@ Xiaoye Lu @@aut@@ Changqing Zhu @@aut@@ Hao Gong @@aut@@ Weiqiang Yang @@aut@@
publishDateDaySort_date	2021-01-01T00:00:00Z
hierarchy_top_id	686948351
id	DOAJ070169357
language_de	englisch
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callnumber-first	Q - Science
author	Lei Tian
spellingShingle	Lei Tian misc QH301-705.5 misc acute kidney injury misc cardiac arrest misc cardiopulmonary resuscitation misc ERK misc levosimendan misc Biology (General) Renoprotective effects of levosimendan on acute kidney injury following cardiac arrest via anti‐inflammation, anti‐apoptosis, and ERK activation
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topic_title	QH301-705.5 Renoprotective effects of levosimendan on acute kidney injury following cardiac arrest via anti‐inflammation, anti‐apoptosis, and ERK activation acute kidney injury cardiac arrest cardiopulmonary resuscitation ERK levosimendan
topic	misc QH301-705.5 misc acute kidney injury misc cardiac arrest misc cardiopulmonary resuscitation misc ERK misc levosimendan misc Biology (General)
topic_unstemmed	misc QH301-705.5 misc acute kidney injury misc cardiac arrest misc cardiopulmonary resuscitation misc ERK misc levosimendan misc Biology (General)
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title	Renoprotective effects of levosimendan on acute kidney injury following cardiac arrest via anti‐inflammation, anti‐apoptosis, and ERK activation
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title_full	Renoprotective effects of levosimendan on acute kidney injury following cardiac arrest via anti‐inflammation, anti‐apoptosis, and ERK activation
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title_sort	renoprotective effects of levosimendan on acute kidney injury following cardiac arrest via anti‐inflammation, anti‐apoptosis, and erk activation
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title_auth	Renoprotective effects of levosimendan on acute kidney injury following cardiac arrest via anti‐inflammation, anti‐apoptosis, and ERK activation
abstract	ATP‐sensitive potassium channels (KATPs) have protective effects in ischemia–reperfusion‐induced injuries and can be activated by levosimendan. This study investigated the effects of levosimendan on renal injury, inflammation, apoptosis, and survival in a rat model of acute kidney injury (AKI) following cardiac arrest (CA) and cardiopulmonary resuscitation (CPR). Rats underwent a 5‐min asphyxia‐based CA and resuscitation. The rats were treated with levosimendan after successful resuscitation. Renal functions, histological changes, inflammatory responses, and apoptosis were examined. NRK‐52E cells treated by hypoxia/reoxygenation (H/R) were used to establish an in vitro CA‐CPR model. Rats in the CA‐induced AKI group had a low survival rate and increased levels of creatinine, blood urea nitrogen, and proinflammatory cytokines, as well as increased tubular injury. These results were significantly reversed after treatment with levosimendan. Levosimendan downregulated the expression of the apoptosis‐related proteins Bax, cleaved caspase‐3, and cleaved caspase‐9, as well as upregulated Bcl‐2 and p‐ERK expression in vivo and in vitro. Thus, our data suggest that levosimendan reduces mortality and AKI following CA and CPR via suppression of inflammation and apoptosis, and activation of ERK signaling.
abstractGer	ATP‐sensitive potassium channels (KATPs) have protective effects in ischemia–reperfusion‐induced injuries and can be activated by levosimendan. This study investigated the effects of levosimendan on renal injury, inflammation, apoptosis, and survival in a rat model of acute kidney injury (AKI) following cardiac arrest (CA) and cardiopulmonary resuscitation (CPR). Rats underwent a 5‐min asphyxia‐based CA and resuscitation. The rats were treated with levosimendan after successful resuscitation. Renal functions, histological changes, inflammatory responses, and apoptosis were examined. NRK‐52E cells treated by hypoxia/reoxygenation (H/R) were used to establish an in vitro CA‐CPR model. Rats in the CA‐induced AKI group had a low survival rate and increased levels of creatinine, blood urea nitrogen, and proinflammatory cytokines, as well as increased tubular injury. These results were significantly reversed after treatment with levosimendan. Levosimendan downregulated the expression of the apoptosis‐related proteins Bax, cleaved caspase‐3, and cleaved caspase‐9, as well as upregulated Bcl‐2 and p‐ERK expression in vivo and in vitro. Thus, our data suggest that levosimendan reduces mortality and AKI following CA and CPR via suppression of inflammation and apoptosis, and activation of ERK signaling.
abstract_unstemmed	ATP‐sensitive potassium channels (KATPs) have protective effects in ischemia–reperfusion‐induced injuries and can be activated by levosimendan. This study investigated the effects of levosimendan on renal injury, inflammation, apoptosis, and survival in a rat model of acute kidney injury (AKI) following cardiac arrest (CA) and cardiopulmonary resuscitation (CPR). Rats underwent a 5‐min asphyxia‐based CA and resuscitation. The rats were treated with levosimendan after successful resuscitation. Renal functions, histological changes, inflammatory responses, and apoptosis were examined. NRK‐52E cells treated by hypoxia/reoxygenation (H/R) were used to establish an in vitro CA‐CPR model. Rats in the CA‐induced AKI group had a low survival rate and increased levels of creatinine, blood urea nitrogen, and proinflammatory cytokines, as well as increased tubular injury. These results were significantly reversed after treatment with levosimendan. Levosimendan downregulated the expression of the apoptosis‐related proteins Bax, cleaved caspase‐3, and cleaved caspase‐9, as well as upregulated Bcl‐2 and p‐ERK expression in vivo and in vitro. Thus, our data suggest that levosimendan reduces mortality and AKI following CA and CPR via suppression of inflammation and apoptosis, and activation of ERK signaling.
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title_short	Renoprotective effects of levosimendan on acute kidney injury following cardiac arrest via anti‐inflammation, anti‐apoptosis, and ERK activation
url	https://doi.org/10.1002/2211-5463.13227 https://doaj.org/article/432c7339c3a44bcb8837d971d8ec1408 https://doaj.org/toc/2211-5463
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This study investigated the effects of levosimendan on renal injury, inflammation, apoptosis, and survival in a rat model of acute kidney injury (AKI) following cardiac arrest (CA) and cardiopulmonary resuscitation (CPR). Rats underwent a 5‐min asphyxia‐based CA and resuscitation. The rats were treated with levosimendan after successful resuscitation. Renal functions, histological changes, inflammatory responses, and apoptosis were examined. NRK‐52E cells treated by hypoxia/reoxygenation (H/R) were used to establish an in vitro CA‐CPR model. Rats in the CA‐induced AKI group had a low survival rate and increased levels of creatinine, blood urea nitrogen, and proinflammatory cytokines, as well as increased tubular injury. These results were significantly reversed after treatment with levosimendan. Levosimendan downregulated the expression of the apoptosis‐related proteins Bax, cleaved caspase‐3, and cleaved caspase‐9, as well as upregulated Bcl‐2 and p‐ERK expression in vivo and in vitro. 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Renoprotective effects of levosimendan on acute kidney injury following cardiac arrest via anti‐inflammation, anti‐apoptosis, and ERK activation

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