Sevoflurane protects the liver from ischemia-reperfusion injury by regulating Nrf2/HO-1 pathway

Ma, Hongyan; Yang, Baoyi; Yu, Li; Gao, Yang; Ye, Xiangmei; Liu, Ying; Li, Zhengtian; Li, Hulun; Li, Enyou

doi:10.1016/j.ejphar.2021.173932

Cited by 19 publications

(12 citation statements)

References 37 publications

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“…Nrf2 is one of the targets of miR-122 (26). Evidence showed that the mitigation effect of sevoflurane on liver IR injury was implicated in the activation of the Nrf2/ HO-1 pathway (27). The Nrf2/HO-1 pathway has both anti-inflammatory and anti-oxidant capabilities and is an important signaling pathway for the body to resist oxidative stress damage.…”

Section: Discussionmentioning

confidence: 99%

Sevoflurane attenuates hepatic ischemia reperfusion injury by the miR-122/Nrf2 pathway

Zhang

2022

Ann Transl Med

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Background: Sevoflurane can protect organs from ischemia-reperfusion (IR) injury, but the mechanism is still unclear. is a liver-specific microRNA (miRNA) and regulates liver function.Therefore, this study aims to elucidate the relationship between the protective effect of sevoflurane and miR-122 in liver IR injury.Methods: Wistar rats were divided into the following groups: sham, IR, IR + sevoflurane, IR + miR-122 antagomir, and IR + miR-122 antagomir + sevoflurane. Hematoxylin and eosin (H&E) staining and Suzuki score were used to evaluate the pathological damage of the liver. The levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-10 in the serum and the levels of malondialdehyde (MDA), superoxide dismutase (SOD), and nitric oxide (NO) in the liver homogenate supernatant were detected by using the corresponding kit. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling (TUNEL) and flow cytometry was applied to evaluate the apoptosis of liver tissues. The expression of nuclear factor E2-related factor 2 (Nrf2), miR-122, p53, and HO-1 in liver tissue was evaluated by using immunohistochemistry, qRT-PCR, and western blot as needed.Results: Compared to the IR group, the sevoflurane post-treatment or miR-122 antagomir groups showed improved liver injury, decreased Suzuki score, inhibited the levels of AST, ALT, LDH, MDA, NO, TNF-α, IL-1β, and IL-6, increased levels of SOD, IL-10, and inhibited hepatocyte apoptosis. Regarding the molecular mechanism, sevoflurane post-treatment fostered the expression of HO-1, promoted the transport of Nrf2 from cytoplasm to the nucleus, and decreased the expression of miR-122 and p53. The combined use of miR-122 antagomir and sevoflurane enhanced the protective effect of miR-122 antagomir in liver injury in IR rats.Conclusions: Sevoflurane protected the liver from IR damage by regulating the miR-122/Nrf2/HO-1 pathway.

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Section: Discussionmentioning

confidence: 99%

Sevoflurane attenuates hepatic ischemia reperfusion injury by the miR-122/Nrf2 pathway

Zhang

2022

Ann Transl Med

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“…Different strategies that could effectively activate Nrf2/HO-1 pathway proved to lead a better outcome during hepatic IR. Table 2 shows several compounds that, by activating Nrf2 signaling pathways, protect the liver from IR injury [48,116,[121][122][123][124][125][126][127][128].…”

Section: Targeting Nrf2: New Opportunities For Liver Ir Protectionmentioning

confidence: 99%

“…Bardoxolone‐Methyl binds to Keap1, inhibits the Keap1‐Nrf2 interaction, leading to the activation of NRF2 as a transcription factor. Sevoflurane, a volatile anesthetic, used as a pre‐ and post‐conditioning agent, exhibits protective effects against liver IR injury [125] through a mechanism related to the Nrf2/HO‐1 pathway regulation [126].…”

Section: Targeting Nrf2: New Opportunities For Liver Ir Protectionmentioning

confidence: 99%

Nrf2 and oxidative stress in liver ischemia/reperfusion injury

et al. 2022

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In response to stress signal, nuclear factor‐erythroid 2‐related factor 2 (Nrf2) induces the expression of target genes involved in antioxidant defense and detoxification. Nrf2 activity is strictly regulated through a variety of mechanisms, including regulation of Keap1‐Nrf2 stability, transcriptional regulation (NF‐ĸB, ATF3, ATF4), and post‐transcriptional regulation (miRNA), evidencing that transcriptional responses of Nrf2 are critical for the maintenance of homeostasis. Ischemia‐reperfusion (IR) injury is a major cause of graft loss and dysfunction in clinical transplantation and organ resection. During the IR process, the generation of reactive oxygen species (ROS) leads to damage from oxidative stress, oxidation of biomolecules, and mitochondrial dysfunction. Oxidative stress can trigger apoptotic and necrotic cell death. Stress factors also result in the assembly of the inflammasome protein complex and the subsequent activation and secretion of proinflammatory cytokines. After Nrf2 activation, the downstream antioxidant upregulation can act as a primary cellular defense against the cytotoxic effects of oxidative stress and help to promote hepatic recovery during IR. The complex crosstalk between Nrf2 and cellular pathways in liver IR injury and the potential therapeutic target of the Nrf2 inducers will be discussed in the present review.

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“…Mitophagy (a special type of autophagy that degrades damaged mitochondria [ 91 ]) protects hepatic cells from reperfusion injury. Activation of the Nrf2/HO-1 axis has been reported to reduce inflammation and oxidative stress and induce autophagy in mouse and rat models of I/R injury [ 92 , 93 , 94 ].…”

Section: Autophagy In Mafldmentioning

confidence: 99%

Autophagy Dysregulation in Metabolic Associated Fatty Liver Disease: A New Therapeutic Target

Chen

Lin

2022

IJMS

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Metabolic associated fatty liver disease (MAFLD) is one of the most common causes of chronic liver disease worldwide. To date, there is no FDA-approved treatment, so there is an urgent need to determine its pathophysiology and underlying molecular mechanisms. Autophagy is a lysosomal degradation pathway that removes damaged organelles and misfolded proteins after cell injury through endoplasmic reticulum stress or starvation, which inhibits apoptosis and promotes cell survival. Recent studies have shown that autophagy plays an important role in removing lipid droplets from hepatocytes. Autophagy has also been reported to inhibit the production of pro-inflammatory cytokines and provide energy for the hepatic stellate cells activation during liver fibrosis. Thyroid hormone, irisin, melatonin, hydrogen sulfide, sulforaphane, DA-1241, vacuole membrane protein 1, nuclear factor erythroid 2-related factor 2, sodium-glucose co-transporter type-2 inhibitors, immunity-related GTPase M, and autophagy-related gene 7 have been reported to ameliorate MAFLD via autophagic induction. Lipid receptor CD36, SARS-CoV-2 Spike protein and leucine aminopeptidase 3 play a negative role in the autophagic function. This review summarizes recent advances in the role of autophagy in MAFLD. Autophagy modulates major pathological changes, including hepatic lipid metabolism, inflammation, and fibrosis, suggesting the potential of modulating autophagy for the treatment of MAFLD.

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Sevoflurane protects the liver from ischemia-reperfusion injury by regulating Nrf2/HO-1 pathway

Cited by 19 publications

References 37 publications

Sevoflurane attenuates hepatic ischemia reperfusion injury by the miR-122/Nrf2 pathway

Sevoflurane attenuates hepatic ischemia reperfusion injury by the miR-122/Nrf2 pathway

Nrf2 and oxidative stress in liver ischemia/reperfusion injury

Autophagy Dysregulation in Metabolic Associated Fatty Liver Disease: A New Therapeutic Target

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