Protective effects of sevoflurane in hepatic ischemia-reperfusion injury

Li, Ji; Yuan, Tong; Zhao, Xin; Lv, Guoyue; Liu, Huan‐Qiu

doi:10.1177/0394632016638346

Cited by 49 publications

(48 citation statements)

References 35 publications

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“…Furthermore, propofol promotes the phosphorylation of mitochondrial glycogen synthase kinase (GSK)‐3β at Ser9, thus consequently restraining the opening of MPT and MMP collapse . Sevoflurane pre‐treatment decreases the release of heparan sulphate and syndecan‐1 and attenuates the release of serum aminopherases in a time‐dependent manner, thus decreasing the shedding of endothelial glycocalyx and cell death rate .…”

Section: Pharmacological Pre‐conditioning Before Hepatic Irmentioning

confidence: 99%

Pre‐conditions for eliminating mitochondrial dysfunction and maintaining liver function after hepatic ischaemia reperfusion

Hu¹

2017

J Cellular Molecular Medi

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The liver, the largest organ with multiple synthesis and secretion functions in mammals, consists of hepatocytes and Kupffer, stem, endothelial, stellate and other parenchymal cells. Because of early and extensive contact with the external environment, hepatic ischaemia reperfusion (IR) may result in mitochondrial dysfunction, autophagy and apoptosis of cells and tissues under various pathological conditions. Because the liver requires a high oxygen supply to maintain normal detoxification and synthesis functions, it is extremely susceptible to ischaemia and subsequent reperfusion with blood. Consequently, hepatic IR leads to acute or chronic liver failure and significantly increases the total rate of morbidity and mortality through multiple regulatory mechanisms. An increasing number of studies indicate that mitochondrial structure and function are impaired after hepatic IR, but that the health of liver tissues or liver grafts can be effectively rescued by attenuation of mitochondrial dysfunction. In this review, we mainly focus on the subsequent therapeutic interventions related to the conservation of mitochondrial function involved in mitigating hepatic IR injury and the potential mechanisms of protection. Because mitochondria are abundant in liver tissue, clarification of the regulatory mechanisms between mitochondrial dysfunction and hepatic IR should shed light on clinical therapies for alleviating hepatic IR‐induced injury.

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Section: Pharmacological Pre‐conditioning Before Hepatic Irmentioning

confidence: 99%

Pre‐conditions for eliminating mitochondrial dysfunction and maintaining liver function after hepatic ischaemia reperfusion

Hu¹

2017

J Cellular Molecular Medi

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“…However, the effect of GRP78 in hepatic ischemia–reperfusion still needs further investigation. As an inhalation anesthetic, sevoflurane has been reported not only with the anesthetic effect, but also significantly reduce hepatic ischemia–reperfusion injury [ 14 ]. Previous studies suggest that the mechanism of sevoflurane on protecting ischemia–reperfusion injury was related to a variety of physiological processes, such as reducing oxygen free radicals, inhibiting inflammatory reaction, reducing intracellular calcium overload as well as improving the energy metabolism of liver cells [ 15 , 16 ].…”

Section: Introductionmentioning

confidence: 99%

Sevoflurane relieves hepatic ischemia–reperfusion injury by inhibiting the expression of Grp78

Liu¹,

Jin²,

Zhang³

et al. 2018

Bioscience Reports

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Purpose: This article aimed to study the role of sevoflurane pre-conditioning in hepatic ischemia–reperfusion and its potential mechanism.Methods: Rat liver ischemia–reperfusion model was constructed. Serum TNF-α, IL-1β, IL-10, and IL-6 concentrations were detected by ELISA. Malondialdehyde (MDA), superoxide dismutase (SOD), and nitric oxide (NO) in liver homogenate were determined. Hematoxylin–Eosin (HE) staining, Tunel, and immunohistochemistry were performed. Ischemia–reperfusion hepatocyte model was established. Cells transfection was conducted. Apoptosis was observed by flow cytometry. Quantitative real-time PCR (qRT-PCR) and Western blotting analysis were used.Results: Compared with I/R group, liver damage degree, liver cell apoptosis, and glucose regulatory protein 78 (Grp78) expression was obviously reduced in rats of SEV group. TNF-α, IL-1β, and IL-6 concentrations were also significantly increased (P<0.01). MDA and NO concentrations were dramatically lower (P<0.01) and SOD concentration was significantly higher (P<0.01). Apoptosis rate, Grp78, PERK, eIF2α, and p-c-JNK/JNK expression was also significantly decreased (P<0.01). Sevoflurane significantly reduced apoptosis and expression of PERK, eIF2α, p-c-JNK/JNK by inhibiting the expression of Grp78 (P<0.01).Conclusion: Sevoflurane relieves hepatic ischemia–reperfusion injury by inhibiting the expression of Grp78.

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“…In a study on Sprague–Dawley rats, Li et al . 113 showed sevoflurane reduced the shedding of HS and SDC1, and preserved the endothelial GCX in the liver following hepatic ischemia. The mechanisms by which sevoflurane inhibitis GCX shedding in IR are not well understood.…”

Section: Part B: the Role Of The Glycocalyx In Vascular Related Diseamentioning

confidence: 92%

The Glycocalyx and Its Role in Vascular Physiology and Vascular Related Diseases

Weinbaum

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et al. 2020

Cardiovasc Eng Tech

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Purpose In 2007 the two senior authors wrote a review on the structure and function of the endothelial glycocalyx layer (Weinbaum in Annu Rev Biomed Eng 9:121–167, 2007). Since then there has been an explosion of interest in this hydrated gel-like structure that coats the luminal surface of endothelial cells that line our vasculature due to its important functions in (A) basic vascular physiology and (B) vascular related diseases. This review will highlight the major advances that have occurred since our 2007 paper. Methods A literature search mainly focusing on the role of the glycocalyx in the two major areas described above was performed using electronic databases. Results In part (A) of this review, the new formulation of the century old Starling principle, now referred to as the Michel–Weinbaum glycoclayx model or revised Starling hypothesis, is described including new subtleties and physiological ramifications. New insights into mechanotransduction and release of nitric oxide due to fluid shear stress sensed by the glycocalyx are elaborated. Major advances in understanding the organization and function of glycocalyx components, and new techniques for measuring both its thickness and spatio-chemical organization based on super resolution, stochastic optical reconstruction microscopy (STORM) are presented. As discussed in part (B) of this review, it is now recognized that artery wall stiffness associated with hypertension and aging induces glycocalyx degradation, endothelial dysfunction and vascular disease. In addition to atherosclerosis and cardiovascular diseases, the glycocalyx plays an important role in lifestyle related diseases (e.g., diabetes) and cancer. Infectious diseases including sepsis, Dengue, Zika and Corona viruses, and malaria also involve the glycocalyx. Because of increasing recognition of the role of the glycocalyx in a wide range of diseases, there has been a vigorous search for methods to protect the glycocalyx from degradation or to enhance its synthesis in disease environments. Conclusion As we have seen in this review, many important developments in our basic understanding of GCX structure, function and role in diseases have been described since the 2007 paper. The future is wide open for continued GCX research.

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Protective effects of sevoflurane in hepatic ischemia-reperfusion injury

Cited by 49 publications

References 35 publications

Pre‐conditions for eliminating mitochondrial dysfunction and maintaining liver function after hepatic ischaemia reperfusion

Pre‐conditions for eliminating mitochondrial dysfunction and maintaining liver function after hepatic ischaemia reperfusion

Sevoflurane relieves hepatic ischemia–reperfusion injury by inhibiting the expression of Grp78

The Glycocalyx and Its Role in Vascular Physiology and Vascular Related Diseases

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