Sevoflurane preconditioning activates HGF/Met-mediated autophagy to attenuate hepatic ischemia-reperfusion injury in mice

Xiao, Xiaoyu; Liu, Dezhao; Chen, Sufang; Li, Xiang; Ge, Mian; Huang, Wenqi

doi:10.1016/j.cellsig.2021.109966

Cited by 11 publications

(17 citation statements)

References 38 publications

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“…In this case, the effect seemed to be more pronounced with IFNγ pre-conditioning at 1 h, while no differences were noticed at 4 h of reperfusion. This finding is in strong accordance with previous data from the literature, suggesting that HGF-met signaling activation in reperfused livers attenuates the damage from IRI [ 31 ]. Moreover, we tested whether the effect of pre-conditioning somehow affected the pro-inflammatory phenotype also at the protein level by measuring the cytokines concentration released in the CM.…”

Section: Resultssupporting

confidence: 93%

“…However, hAMSCs priming with the IFNγ or 3D culture condition strongly reduced the expression of IL-1β, IL-12 and PTSG2. Notably, the HGF up-regulation in the same samples is consistent with previous findings showing the HGF-Met signaling axis as protective towards liver IRI [ 31 ]. In addition, the ELISA analysis on the 3D hAMSC-CM and γ-hAMSC-CM from reperfused macrophages showed an increased release of IL-13 after reperfusion.…”

Section: Discussionsupporting

confidence: 91%

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Human Amnion-Derived Mesenchymal Stromal/Stem Cells Pre-Conditioning Inhibits Inflammation and Apoptosis of Immune and Parenchymal Cells in an In Vitro Model of Liver Ischemia/Reperfusion

Zito

Miceli

Carcione

et al. 2022

Cells

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Ischemia/reperfusion injury (IRI) represents one of the leading causes of primary non-function acute liver transplantation failure. IRI, generated by an interruption of organ blood flow and the subsequent restoration upon transplant, i.e., reperfusion, generates the activation of an inflammatory cascade from the resident Kupffer cells, leading first to neutrophils recruitment and second to apoptosis of the parenchyma. Recently, human mesenchymal stromal/stem cells (hMSCs) and derivatives have been implemented for reducing the damage induced by IRI. Interestingly, sparse data in the literature have described the use of human amnion-derived MSCs (hAMSCs) and, more importantly, no evidence regarding hMSCs priming on liver IRI have been described yet. Thus, our study focused on the definition of an in vitro model of liver IRI to test the effect of primed hAMSCs to reduce IRI damage on immune and hepatic cells. We found that the IFNγ pre-treatment and 3D culture of hAMSCs strongly reduced inflammation induced by M1-differentiated macrophages. Furthermore, primed hAMSCs significantly inhibited parenchymal apoptosis at early timepoints of reperfusion by blocking the activation of caspase 3/7. All together, these data demonstrate that hAMSCs priming significantly overcomes IRI effects in vitro by engaging the possibility of defining the molecular pathways involved in this process.

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Section: Resultssupporting

confidence: 93%

Section: Discussionsupporting

confidence: 91%

Human Amnion-Derived Mesenchymal Stromal/Stem Cells Pre-Conditioning Inhibits Inflammation and Apoptosis of Immune and Parenchymal Cells in an In Vitro Model of Liver Ischemia/Reperfusion

Zito

Miceli

Carcione

et al. 2022

Cells

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“…In addition to its anesthetic properties, SEV has been reported to inhibit inflammation and apoptosis during sepsis to protect against organ's injury including brain, 5,6 lung, 7 heart, 8 and liver. 9 For example, SEV was found to exert brain-protective effects on sepsis via regulating apoptosis-related signaling pathway in a rat model with sepsis. 5 SEV showed a cytoprotective effect in human umbilical vein endothelial cells with LPS stimulation through decreasing cell death and reducing the releases of the inflammatory mediators TNF-α and IL-6.…”

Section: Western Blotting Assaymentioning

confidence: 99%

“…For the establishment of SI-AKI cell model, HK-2 cells were stimulated with 10 μg/mL LPS (Sigma) for 24 h. 23 For SEV treatment, cells were pre-treated with 2.4% SEV (Sigma) for 1 h. 9,24 To inhibit SIRT1, LPS plus SEV-treated HK-2 cell line was co-treated with 10 μM EX527 (MedChem Express), an inhibitor of SIRT1, for 24 h. 25…”

Section: Introductionmentioning

confidence: 99%

Sevoflurane ameliorates LPS-induced inflammatory injury of HK-2 cells through Sirtuin1/NF-κB pathway

Wang

Yin

et al. 2022

Allergol Immunopathol

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The anesthetic sevoflurane (SEV) has been shown to protect against organ’s injury during sepsis. The present study intended to uncover the protective effects of SEV on sepsis-induced acute kidney injury (SI-AKI) and its possible mechanism. Human renal tubular epithelial cell HK-2 was treated with 10 μg/mL lipopolysaccharide (LPS) to construct SI-AKI cell model. LPS-induced HK-2 cells were pretreated with SEV in the absence or presence of EX527, an inhibitor of Sirtuin 1 (SIRT1), after which were the detection of cell viability, lactate dehydrogenase (LDH) release, apoptosis, inflammation, and oxidative stress. Our results demonstrated that LPS caused decreased cell viability, increased LDH release, improved cell apoptosis along with decreased expression of Bcl2 and enhanced expressions of Bax, cleaved PARP and cleaved caspase, enhanced production, and protein expressions of TNF-α, IL-6, and IL-1β, increased generation of reactive oxygen species (ROS) and malondialdehyde (MDA), but contributed to declined activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). LPS inhibited SIRT1 and IκBα expressions but upregulated p-NF-κB p65 and acetyl-p53 expressions as well. However, SEV pretreatment abolished all above-mentioned effects of LPS on HK-2 cells, while EX527 significantly reversed the effects of SEV. In conclusion, SEV effectively protected HK-2 cells against LPS-induced apoptosis, inflammation, and oxidative stress, and these effects may depend on the increase of SIRT1 expression, thereby inactivating NF-κB signaling.

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“…Several studies have demonstrated that inhibiting oxidative stress could alleviate the development of acute liver injury, indicating that antioxidant agents might be effective strategies for the treatment of acute liver injury [ 4 , 5 ]. Autophagy is a homeostatic degradative process that could clear the misfolded proteins and damaged organelles, and is involved in the progression of various liver diseases [ 6 , 7 ]. Recent findings have suggested that defective autophagy in liver is often be detected during the pathogenesis of acute liver injury, and that the reactivation of autophagy could be an effective therapy for the prevention of acute liver failure [ 8 , 9 ].…”

Section: Introductionmentioning

confidence: 99%

Alanyl-Glutamine Protects against Lipopolysaccharide-Induced Liver Injury in Mice via Alleviating Oxidative Stress, Inhibiting Inflammation, and Regulating Autophagy

Ying

Zheng

et al. 2022

Antioxidants

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Acute liver injury is a worldwide problem with a high rate of morbidity and mortality, and effective pharmacological therapies are still urgently needed. Alanyl-glutamine (Ala-Gln), a dipeptide formed from L-alanine and L-glutamine, is known as a protective compound that is involved in various tissue injuries, but there are limited reports regarding the effects of Ala-Gln in acute liver injury. This present study aimed to investigate the protective effects of Ala-Gln in lipopolysaccharide (LPS)-induced acute liver injury in mice, with a focus on inflammatory responses and oxidative stress. The acute liver injury induced using LPS (50 μg/kg) and D-galactosamine (D-Gal) (400 mg/kg) stimulation in mice was significantly attenuated after Ala-Gln treatment (500 and 1500 mg/kg), as evidenced by reduced plasma alanine transaminase (ALT) (p < 0.01, p < 0.001), aspartate transaminase (AST) (p < 0.05, p < 0.001), and lactate dehydrogenase (LDH) (p < 0.01, p < 0.001) levels, and accompanied by improved histopathological changes. In addition, LPS/D-Gal-induced hepatic apoptosis was also alleviated by Ala-Gln administration, as shown by a greatly decreased ratio of TUNEL-positive hepatocytes, from approximately 10% to 2%, and markedly reduced protein levels of cleaved caspase-3 (p < 0.05, p < 0.001) in liver. Moreover, we found that LPS/D-Gal-triggered oxidative stress was suppressed after Ala-Gln treatment, the effect of which might be dependent on the elevation of SOD and GPX activities, and on GSH levels in liver. Interestingly, we observed that Ala-Gln clearly inhibited LPS/D-Gal exposure-induced macrophage accumulation and the production of proinflammatory factors in the liver. Furthermore, Ala-Gln greatly regulated autophagy in the liver in LPS/D-Gal-treated mice. Using RAW264.7 cells, we confirmed the anti-inflammatory role of Ala-Gln-targeting macrophages.

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Sevoflurane preconditioning activates HGF/Met-mediated autophagy to attenuate hepatic ischemia-reperfusion injury in mice

Cited by 11 publications

References 38 publications

Human Amnion-Derived Mesenchymal Stromal/Stem Cells Pre-Conditioning Inhibits Inflammation and Apoptosis of Immune and Parenchymal Cells in an In Vitro Model of Liver Ischemia/Reperfusion

Human Amnion-Derived Mesenchymal Stromal/Stem Cells Pre-Conditioning Inhibits Inflammation and Apoptosis of Immune and Parenchymal Cells in an In Vitro Model of Liver Ischemia/Reperfusion

Sevoflurane ameliorates LPS-induced inflammatory injury of HK-2 cells through Sirtuin1/NF-κB pathway

Alanyl-Glutamine Protects against Lipopolysaccharide-Induced Liver Injury in Mice via Alleviating Oxidative Stress, Inhibiting Inflammation, and Regulating Autophagy

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