Protective effects of therapeutic hypothermia on renal injury in an asphyxial cardiac arrest rat model

Islam, Anowarul; Kim, So Eun; Yoon, Jae Chol; Ali, Jawad; Tian, Weishun; Yoo, Yeo-Jin; Kim, In-Shik; Ahn, Dongchoon; Park, Byung-Yong; Hwang, Yong Gyoo; Lee, Jehee; Tae, Hyun‐Jin; Cho, Jeong‐Hwi; Kim, Kyung-Hwa

doi:10.1016/j.jtherbio.2020.102761

Cited by 4 publications

(12 citation statements)

References 34 publications

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“…In the reperfusion process, highly electrophilic ROS outburst results in perturbing renal redox balance state, that directly causes the breakdown of DNA, inactivation of protein, renal structural and functional tubular cell damage by extensive membrane lipid peroxidation 19 . In this study, MDA significantly increased in CA-operated groups compared to the sham group and showed similarity with the previous results of RI/RI 6 , 20 . Therefore, the present study suggests that our asphyxial CA involvesRI/RI mechanism resulting in oxidative stress induction and provokes renal damage 20 .…”

Section: Discussionsupporting

confidence: 91%

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

et al. 2021

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To investigate the role of Nrf2/HO-1 in renal histopathological ailments time-dependently in asphyxial cardiac arrest (CA) rat model. Methods: Eighty-eight Sprague Dawley male rats were divided into five groups of eight rats each. Asphyxial CA was induced in all the experimental rats except for the sham group. The rats were sacrificed at 6 hours, 12 hours, one day and two days post-CA. Serum blood urea nitrogen (BUN), creatinine (Crtn) and malondialdehyde from the renal tissues were evaluated. Hematoxylin and eosin and periodic acid-Schiff staining were done to evaluate the renal histopathological changes in the renal cortex. Furthermore, Nrf2/HO-1 immunohistochemistry (ihc) and western blot analysis were performed after CA. Results: The survival rate of rats decreased in a time-dependent manner: 66.6% at 6 hours, 50% at 12 hours, 38.1% in one day, and 25.8% in two days. BUN and serum Crtn markedly increased in CA-operated groups. Histopathological ailments of the renal cortical tissues increased significantly from 6 hours until two days post-CA. Furthermore, Nrf2/HO-1 expression level significantly increased at 6 hours, 12 hours, and one day. Conclusion: The survival rate decreased time-dependently, and Nrf/HO-1 expression increased from 6 hours with the peak times at 12 hours, and one day post-CA.

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Section: Discussionsupporting

confidence: 91%

“…In this study, MDA significantly increased in CA-operated groups compared to the sham group and showed similarity with the previous results of RI/RI 6 , 20 . Therefore, the present study suggests that our asphyxial CA involvesRI/RI mechanism resulting in oxidative stress induction and provokes renal damage 20 .…”

Section: Discussionsupporting

confidence: 91%

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

et al. 2021

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“…group with 6 h TH immediately after ROSC and rewarming was performed to attain normal temperature, which was maintained until the rats were sacrificed (Hypo 6 h) (n=7). The number of rats in each group was selected according to the expected survival rate of each group with a target of having 6 animals per group at the end of the protocol; in contrast to the estimated high survival rate at 2 and 4 h of TH ( 25 ).…”

Section: Methodsmentioning

confidence: 99%

“…A Leica DM 2500 microscope (Leica Microsystems) was used to image the sections at fixed magnifications of x400 (H&E) and x1,000 (PAS), and in each group, 10 specific areas were captured. Analysis of glomerular lesions was performed according to a previously published procedure ( 25 ). The scoring was as follows: Normal, 0; <25% damage, 1; 26-50% damage, 2; 51-75% damage, 3; and 76-100% damage, 4( 25 ).…”

Section: Methodsmentioning

confidence: 99%

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Therapeutic hypothermia effect on asphyxial cardiac arrest‑induced renal ischemia/reperfusion injury via change of Nrf2/HO‑1 levels

et al. 2021

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The present study aimed to investigate the renoprotective effect of therapeutic hypothermia (TH) on renal ischemia-reperfusion injury (RI/RI) induced by asphyxial cardiac arrest (CA) in rats. A total of 48 male rats were randomly divided into five groups: i) Sham (n=6); ii) Normothermia + CA (Normo.) (n=14); iii) Normo. and 2 h of TH after return of spontaneous circulation (ROSC) (n=12); iv) Normo. and 4 h of TH after ROSC (n=9); and v) Normo. and 6 h of TH after ROSC (n=7). All rats except the Sham group underwent asphyxia CA and were sacrificed 1 day after ROSC. The survival rate increased from 42.8% in the Normo. group to 50, 66.6 and 85.7% in the groups with 2, 4 and 6 h of TH after CA, respectively. TH attenuated the histopathological changes of the renal tissues following ROSC and the levels of blood urea nitrogen, serum creatinine and malondialdehyde in renal tissues. On immunohistochemistry, the relative optical density of nuclear erythroid-related factor-2 (Nrf2) and heme oxygenase (HO-1) expression in renal tissues increased in the Normo. group compared with that in the Sham group and exhibited further significant increases at 6 h of TH after ROSC. In conclusion, TH attenuated renal injury and increased the expression of Nrf2 and HO-1 in a TH treatment time-dependent manner.

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Risperidone Administration Attenuates Renal Ischemia and Reperfusion Injury following Cardiac Arrest by Antiinflammatory Effects in Rats

Kim

Lee

et al. 2023

Veterinary Sciences

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Multi-organ dysfunction following cardiac arrest is associated with poor outcome as well as high mortality. The kidney, one of major organs in the body, is susceptible to ischemia and reperfusion; however, there are few studies on renal ischemia and reperfusion injury (IRI) following the return of spontaneous circulation (ROSC) after cardiac arrest. Risperidone, an atypical antipsychotic drug, has been discovered to have some beneficial effects beyond its original effectiveness. Therefore, the aim of the present study was to investigate possible therapeutic effects of risperidone on renal IRI following cardiac arrest. Rats were subjected to cardiac arrest induced by asphyxia for five minutes followed by ROSC. When serum biochemical analyses were examined, the levels of serum blood urea nitrogen, creatinine, and lactate dehydrogenase were dramatically increased after cardiac arrest, but they were significantly reduced by risperidone administration. Histopathology was examined using hematoxylin and eosin staining. Histopathological injury induced by cardiac arrest was apparently attenuated by risperidone administration. Furthermore, alterations in pro-inflammatory cytokines (interleukin-6 and tumor necrosis factor-α) and anti-inflammatory cytokines (interleukin-4 and interleukin-13) were examined by immunohistochemistry. Pro-inflammatory and anti-inflammatory cytokine immunoreactivities were gradually and markedly increased and decreased, respectively, in the kidneys following cardiac arrest; however, risperidone administration after cardiac arrest significantly attenuated the increased pro-inflammatory cytokine immunoreactivities and the decreased anti-inflammatory cytokine immunoreactivities. Collectively, our current results revealed that, in rats, risperidone administration after cardiac arrest protected kidneys from IRI induced by cardiac arrest and ROSC through anti-inflammatory effects.

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Protective effects of therapeutic hypothermia on renal injury in an asphyxial cardiac arrest rat model

Cited by 4 publications

References 34 publications

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

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

Therapeutic hypothermia effect on asphyxial cardiac arrest‑induced renal ischemia/reperfusion injury via change of Nrf2/HO‑1 levels

Risperidone Administration Attenuates Renal Ischemia and Reperfusion Injury following Cardiac Arrest by Antiinflammatory Effects in Rats

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