Oxidative stress on ischemia/reperfusion injury in mice with non-alcoholic hepatic steatosis or steatohepatitis

Cayuela, Natalie Chaves; Negreti, Gabrielly Pascoa; Rasslan, Roberto; Koike, Márcia Kiyomi; Montero, Edna Frasson de Souza

doi:10.1590/s0102-865020180090000003

Cited by 3 publications

(1 citation statement)

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“…Increased oxidative stress is an important reason for the increase of fatty liver ischemia-reperfusion injury. 15,16 It has been reported that one-hour HOPE treatment before transplantation led to decreased post-transplant oxidative stress, 14 but the exact underlying mechanism is still unclear. As a sensor of intracellular oxidative stress, transcription factor Nrf2 plays an important role in antioxidant stress.…”

Section: Introductionmentioning

confidence: 99%

Hypothermic oxygenated perfusion ameliorates ischemia‐reperfusion injury of fatty liver in mice via Brg1/Nrf2/HO‐1 axis

et al. 2021

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Background: After cold storage (CS) and subsequent transplantation, fatty liver is more inclined to develop liver dysfunction and serious postoperative complications in contrast to healthy liver. Hypothermic oxygenated perfusion (HOPE) is a safe and efficacious system, which can repair fatty liver and reduce ischemiareperfusion injury. The aim of this research is to investigate the function of Brg1/ Nrf2/HO-1 signaling pathway in the protective effect of HOPE on ischemiareperfusion injury of fatty liver. Methods:The mouse fatty liver model was successfully established and verified by hematoxylin-eosin (HE) staining and oil red O staining. The animals were divided into Control group, CS group and HOPE group. The levels of liver enzyme and lactate in the perfusate were used to measure liver function and cellular metabolism. HE staining and TUNEL staining were utilized to assess the tissue structure and apoptosis, respectively. The levels of superoxide dismutase, malondialdehyde and reactive oxygen species in liver tissue were measured to quantitatively analyze the degree of oxidative stress, and the expressions of protein Brg1, Nrf2 and HO-1 were detected by means of the western blot. Double-labeling immunofluorescence was to explore the colocalization of Brg1 and Nrf2. Results:The injury of the liver in the CS group was more serious than that in the control group. However, HOPE could significantly reduce the injury, which was manifested by the improvement of liver function and cellular metabolism, and the lower degrees of apoptosis, necrosis and oxidative stress. Furthermore, the expressions of Brg1, Nrf2 and HO-1 in the HOPE group were significantly increased than those in the CS group. Conclusions:One-hour HOPE treatment before reperfusion can obviously improve the injury of fatty liver in mice. The underlying mechanism may be that the interaction of Brg1 and Nrf2 can selectively activate the transcription of HO-1.

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Section: Introductionmentioning

confidence: 99%