Protective effect of propofol preconditioning on ischemia-reperfusion injury in human hepatocyte

Zhang, Yuzhu; Chen, Zhenzhen; Feng, Nianhai; Zhao, Xianxian; Liu, Chengxiao; Xu, Hongzhou; Zhang, Mengyuan

doi:10.21037/jtd.2017.02.80

Cited by 18 publications

(11 citation statements)

References 44 publications

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“…It has also been found by multiple research teams that propofol has protective effects against IRI in multiple organs [33,34]. Propofol infusion has also been suggested to have protective effects against renal IRI in rats, but the underlying mechanism is not fully understood [10,13,35]. In the present study, HE staining of IRI-affected rat renal tissue (Fig.…”

Section: +supporting

confidence: 55%

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The Protective Effect of Propofol Against Ischemia–Reperfusion Injury in the Interlobar Arteries: Reduction of Abnormal Cx43 Expression as a Possible Mechanism

Chang

Xue

et al. 2018

Kidney Blood Press Res

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Background/Aims: This experimental study aims to observe whether the protective effect of propofol against renal ischemia–reperfusion injury (IRI) in the rat interlobar artery occurs through altered expression of the gap junction protein connexin 43 (Cx43). Methods: This study randomly divided male Sprague Dawley (SD) rats into an untreated control group, a sham-operated control group (sham group), an ischemia–reperfusion group (IR group), a propofol group (propofol+IR group) and a fat emulsion group (Intralipid group). The ischemia/reperfusion model was prepared through resection of the right kidney and noninvasive arterial occlusion of the left kidney. Forty-five minutes after renal ischemia–reperfusion, an automatic biochemical analyzer was employed to measure blood urea nitrogen (BUN) and serum creatinine (SCr); changes in renal tissue pathology were observed using hematoxylin and eosin (HE) staining, and the vasomotor activity of the interlobar artery was detected using a pressure mechanogram technique. The protein expression of Cx43 in renal artery cross-sections was determined through western blotting. Results: The experimental study confirmed that the BUN and SCr of rats markedly increased after ischemia–reperfusion injury; additionally, we observed some coagulation necrosis and shedding of cells, some solidification of nuclear chromatin, degeneration of cytoplasmic vacuoles, high renal interstitial vascular congestion and obvious inflammatory cell infiltration, characterized by focal hemorrhages. Furthermore, the contraction activity of the renal interlobar artery greatly decreased, and the tension of the arteries in the renal lobe increased remarkably. After the gap junction blocking agents 2-APB and Gap27 were applied, the systolic velocity of blood vessels and the vascular contraction rate both decreased. In addition, the expression of Cx43 in kidney tissues increased markedly. The damage was more severe after 24 h of ischemic reperfusion than after only 4 h. However, after pretreatment with propofol, regardless of whether ischemia–reperfusion was applied for 4 h or 24 h, the previously increased expression of Cx43 decreased obviously, and all forms of renal damage were reversed. Conclusion: Our research suggests new ways for propofol to relieve ischemia–reperfusion injury by decreasing the abnormal expression of the gap junction protein Cx43. This study reveals a novel mechanism for the action of propofol against IRI, and we hope this finding will lead to new treatments for IRI.

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Section: +supporting

confidence: 55%

“…In recent years, studies have demonstrated the protective effects of propofol against ischemic injury in the kidneys, liver and heart [9][10][11]. It has been suggested in early studies that propofol protects against opioid-induced hyperresponsiveness of airway smooth muscle during target-controlled infusion anesthesia [12].…”

Section: Introductionmentioning

confidence: 99%

The Protective Effect of Propofol Against Ischemia–Reperfusion Injury in the Interlobar Arteries: Reduction of Abnormal Cx43 Expression as a Possible Mechanism

Chang

Xue

et al. 2018

Kidney Blood Press Res

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“…Studies have found that propofol inhibits the activity of nuclear transcription factor NF-kβ during ischemia reperfusion injury and reduces the adhesion force of endotheliocytes 16 . In addition, propofol inhibits hydrogen peroxide-induced myocardial apoptosis and attenuates myocardial ischemia reperfusion injury by regulating autophagy-related genes 17 – 21 .…”

Section: Introductionmentioning

confidence: 99%

Propofol-induced MiR-20b expression initiates endogenous cellular signal changes mitigating hypoxia/re-oxygenation-induced endothelial autophagy in vitro

Wang

Cai

et al. 2020

Cell Death Dis

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Certain miRNAs can attenuate hypoxia/re-oxygenation-induced autophagic cell death reported in our previous studies, but how these miRNAs regulate the autophagy-related cellular signaling pathway in preventing cell death is largely unknown. In the current study, the autophagy-related miRNAs of hsa-miR-20b were investigated in an in vitro model of hypoxia/re-oxygenation-induced endothelial autophagic cell death. Of these, miR-20b was found to be the most important miRNA which targeted on the key autophagy kinase ULK1 and inhibited hypoxia/re-oxygenation injury-induced autophagy by decreasing both autophagosomes and LC3I to II transition rate and P62 degradation. These processes were reversed by the transfection of an miR-20b inhibitor. Re-expression of ULK1 restores miR-20b-inhibited autophagy. Propofol, a commonly used anesthetic, promoted miR-20b and METTL3 expression and attenuated endothelial autophagic cell death. The inhibited endogenous expression of miR-20b or silenced METTL3 diminished the protective effect of propofol and accentuated autophagy. Additionally, METTL3 knockdown significantly inhibited miR-20b expression but up-regulated pri-miR-20b expression. Together, our data shows that propofol protects against endothelial autophagic cell death induced by hypoxia/re-oxygenation injury, associated with activation of METTL3/miR-20b/ULK1 cellular signaling.

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“…In contrast, due to its phenolic structure, propofol can prevent ischemic/reperfusion injury (13,14). Furthermore, propofol has an anti-oxidative effect in rat cardiomyocytes and macrophages, which is associated with the suppression of oxidative stress-related enzymes including inducible nitric oxide synthase, superoxide dismutase (SOD) and neutrophil cytosolic factor 1.…”

Section: Introductionmentioning

confidence: 99%

Propofol protects human cardiac cells against chemical hypoxiainduced injury by regulating the JNK signaling pathways

et al. 2020

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Propofol is a widely used intravenous anesthetic shown to exert a cardioprotective role against oxidative stress and ischemia/reperfusion injury in rat cardiac H9c2 cells. However, the regulatory mechanisms and functions of propofol in human cardiomyocytes remain unknown. The present study chemically induced hypoxia with cobalt chloride (CoCl 2 ) to mimic cardiomyocyte ischemic injury in human cardiac AC16 and HCM cells. To investigate its underlying mechanisms, propofol was added to the cells before the chemical hypoxia phase. The present results suggested that, in response to hypoxia, mitochondrial membrane potential was lost, and cardiomyocyte viability and superoxide dismutase levels decreased. However, the present results showed that reactive oxygen species and malondialdehyde levels increased. The present results suggested that these effects were significantly reversed following propofol treatment. Additionally, the present results suggested that the protective effect of propofol against CoCl 2 -induced injury may be inhibited by the activation of the JNK signaling pathways. The present results indicated that propofol pre-treatment inhibited CoCl 2 -induced myocardial injury by preventing mitochondrial dysfunction, which may be partially due to the activation of the JNK signaling pathways. Therefore, propofol may exert anti-oxidative effects in human cardiac cells. The present results suggested that propofol may be used as a treatment for oxidative stress-related cardiac disorders.

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Protective effect of propofol preconditioning on ischemia-reperfusion injury in human hepatocyte

Cited by 18 publications

References 44 publications

The Protective Effect of Propofol Against Ischemia–Reperfusion Injury in the Interlobar Arteries: Reduction of Abnormal Cx43 Expression as a Possible Mechanism

The Protective Effect of Propofol Against Ischemia–Reperfusion Injury in the Interlobar Arteries: Reduction of Abnormal Cx43 Expression as a Possible Mechanism

Propofol-induced MiR-20b expression initiates endogenous cellular signal changes mitigating hypoxia/re-oxygenation-induced endothelial autophagy in vitro

Propofol protects human cardiac cells against chemical hypoxiainduced injury by regulating the JNK signaling pathways

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