Changes of renal histopathology and the role of Nrf2/HO-1 in asphyxial cardiac arrest model in rats

Ali, Jawad; Yoo, Yeo-Jin; Yoon, Jae Chol; Tian, Weishun; Islam, Sadikul; Lee, Eui-Yong; Shin, Ha-Young; Kim, So Eun; Ahn, Dongchoon; Park, Byung-Yong; Tae, Hyun‐Jin; Kim, In-Shik

doi:10.1590/acb360607

Cited by 6 publications

(7 citation statements)

References 27 publications

(47 reference statements)

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“…Increased ROS can also lead to MDA generation and severely weaken the antioxidant enzyme system ( 37 ). In the present study, MDA was markedly increased in CA groups compared with the sham group, resembling results of a previous study ( 26 ). Thus, asphyxial CA can increase oxidative stress in a time-dependent manner and provoke renal damage.…”

Section: Discussionsupporting

confidence: 92%

“…In the present study, the survival rate declined in a time-dependent manner, reaching 33% at two days post-CA. Previous studies have also shown the same pattern of survivability ( 25 , 26 ). Therefore, our asphyxial CA model was suitable for studying CA patients.…”

Section: Discussionsupporting

confidence: 73%

“…In the present study, we found severe histological changes in kidney tissues. Jawad et al ( 26 ) and Kim et al ( 19 ) have reported the same pattern of histopathological changes in renal tissues after induction of asphyxial CA. Creatinine and BUN are the most frequently utilized endogenous indicators for assessing glomerular function ( 30 ).…”

Section: Discussionmentioning

confidence: 63%

“…Creatinine and BUN are the most frequently utilized endogenous indicators for assessing glomerular function ( 30 ). These are markedly augmented after ROSC in CA hospital patients and in an induced-CA rat model ( 26 ). Previous studies have also reported that BUN and creatine levels are increased at 1 day and 2 days after ROSC in an asphaxial CA rat model ( 31 , 32 ).…”

Section: Discussionmentioning

confidence: 99%

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Changes of antioxidant enzymes in the kidney after cardiac arrest in the rat model

Lee

Islam

Yoo

et al. 2023

Braz J Med Biol Res

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Globally, cardiac arrest (CA) is a leading cause of death and disability. Asphyxial CA (ACA)-induced kidney damage is a crucial factor in reducing the survival rate. The purpose of this study was to investigate the role of antioxidant enzymes in histopathological renal damage in an ACA rat model at different time points. A total of 88 rats were divided into five groups and exposed to ACA except for the sham group. To evaluate glomerular function and oxidative stress, serum levels of blood urea nitrogen (BUN) and creatinine (Crtn) and malondialdehyde (MDA) levels in renal tissues were measured. To determine histopathological damage, hematoxylin and eosin staining, periodic acid-Schiff staining, and Masson's trichrome staining were performed. Expression levels of antioxidant enzymes including superoxide dismutase-1 (SOD-1), superoxide dismutase-2 (SOD-2), catalase (CAT), and glutathione peroxidase (GPx) were measured by immunohistochemistry (IHC). Survival rate of the experimental rats was reduced to 80% at 6 h, 55% at 12 h, 42.9% at 1 day, and 33% at 2 days after return of spontaneous circulation. Levels of BUN, Crtn, and MDA started to increase significantly in the early period of CA induction. Renal histopathological damage increased markedly from 6 h until two days post-CA. Additionally, expression levels of antioxidant enzymes were significantly decreased at 6 h, 12 h, 1 day, and 2 days after CA. CA-induced oxidative stress and decreased levels of antioxidant enzymes (SOD-1, SOD-2, CAT, GPx) from 6 h to two days could be possible mediators of severe renal tissue damage and increased mortality rate.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 73%

Section: Discussionmentioning

confidence: 63%

Section: Discussionmentioning

confidence: 99%

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Changes of antioxidant enzymes in the kidney after cardiac arrest in the rat model

Lee

Islam

Yoo

et al. 2023

Braz J Med Biol Res

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“…Recently, it has been suggested that Nrf2/HO-1 pathway was activated in the early stage after ROSC. However, the expression of Nrf2/HO-1 decreased, the renal injury and dysfunction increased, and the survival rate of rats decreased during later stage after ROSC ( 50 ). Therefore, the activation of Nrf2/HO-1 pathway may be a promising therapeutic target on post-resuscitation AKI.…”

Section: Discussionmentioning

confidence: 99%

Protection Against Post-resuscitation Acute Kidney Injury by N-Acetylcysteine via Activation of the Nrf2/HO-1 Pathway

et al. 2022

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Background and ObjectiveAcute kidney injury (AKI), the common complication after cardiopulmonary resuscitation (CPR), seriously affects the prognosis of cardiac arrest (CA) patients. However, there are limited studies on post-resuscitation AKI. In addition, it has been demonstrated that N-acetylcysteine (N-AC) as an ROS scavenger, has multiorgan-protective effects on systemic and regional ischaemia-reperfusion injuries. However, no studies have reported its protective effects against post-resuscitation AKI and potential mechanisms. This study aimed to clarify the protective effects of N-AC on post-resuscitation AKI and investigate whether its potential mechanism was mediated by activating Nrf-2/HO-1 pathway in the kidney.MethodsWe established cardiac arrest models in rats. All animals were divided into four groups: the sham, control, N-AC, and ZnPP groups. Animals in each group except for the ZnPP group were assigned into two subgroups based on the survival time: 6 and 48 h. The rats in the control, N-AC, and ZnPP groups underwent induction of ventricular fibrillation (VF), 8 min untreated VF and cardiopulmonary resuscitation. Renal function indicators, were detected using commercial kits. Renal pathologic changes were assessed by haematoxylin–eosin (HE) staining. Oxidative stress and inflammatory responses were measured using the corresponding indicators. Apoptosis was evaluated using terminal uridine nick-end labeling (TUNEL) staining, and expression of proteins associated with apoptosis and the Nrf-2/HO-1 pathway was measured by western blotting.ResultsN-AC inhibited post-resuscitation AKI. We observed that N-AC reduced the levels of biomarkers of renal function derangement; improved renal pathological changes; and suppressed apoptosis, oxidative stress, and inflammatory response. Additionally, the production of ROS in the kidneys markedly decreased by N-AC. More importantly, compared with the control group, N-AC further upregulated the expression of nuclear Nrf2 and endogenous HO-1 in N-AC group. However, N-AC-determined protective effects on post-resuscitation AKI were markedly reversed after pretreatment of the HO-1 inhibitor zinc protoporphyrin (ZnPP).ConclusionsN-AC alleviated renal dysfunction and prolonged survival in animal models of CA. N-AC partially exerts beneficial renal protection via activation of the Nrf-2/HO-1 pathway. Altogether, all these findings indicated that N-AC as a common clinical agent, may have the potentially clinical utility to improve patients the outcomes in cardiac arrest.

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Biliverdin modulates the Nrf2/A20/eEF1A2 axis to alleviate cerebral ischemia-reperfusion injury by inhibiting pyroptosis

Bai

Huo

Zhou

et al. 2023

Biomedicine & Pharmacotherapy

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Changes of renal histopathology and the role of Nrf2/HO-1 in asphyxial cardiac arrest model in rats

Cited by 6 publications

References 27 publications

Changes of antioxidant enzymes in the kidney after cardiac arrest in the rat model

Changes of antioxidant enzymes in the kidney after cardiac arrest in the rat model

Protection Against Post-resuscitation Acute Kidney Injury by N-Acetylcysteine via Activation of the Nrf2/HO-1 Pathway

Biliverdin modulates the Nrf2/A20/eEF1A2 axis to alleviate cerebral ischemia-reperfusion injury by inhibiting pyroptosis

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