Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The endothelial glycocalyx plays a critical role in the regulation of vascular structure and functions. Previous studies have demonstrated that sevoflurane, a volatile anesthetic, can preserve the endothelial glycocalyx in heart tissues against ischemia-reperfusion injury. However, little is known about the effects of sevoflurane pretreatment on the vascular structure and functions of liver tissues following ischemia-reperfusion injury. To this end, female Sprague-Dawley rats (n = 28) were anesthetized either with ketamine (80-120 mg/kg, i.p.) or with one minimum alveolar concentration (MAC) sevoflurane (2% v/v). Following in vivo hepatic ischemia procedure, the liver was isolated and reperfusion was produced. During the period of reperfusion, liver reperfusion samples were collected, and the concentrations of heparan sulfate and syndecan-1 (Syn-1), and the levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) enzymes, were measured. The morphology of hepatocytes and endothelial glycocalyx were then assessed by using the light and electron microscopies, respectively. Ischemia-reperfusion increased the release of HS and Syn-1, and elevated the levels of ALT and AST in a time-dependent manner. However, sevoflurane pretreatment reduced the release of HS and Syn-1and attenuated the levels of ALT and AST, in a time-dependent manner, as compared with ketamine pretreatment. Furthermore, sevoflurane pretreatment decreased the shedding of endothelial glycocalyx and hepatocytes necrosis. Sevoflurane pretreatment preserved the endothelial glycocalyx in the liver tissue against ischemia-reperfusion injury. The effect appears to help protect hepatocytes against ischemia-reperfusion-induced necrosis.
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PMID:Protective effects of sevoflurane in hepatic ischemia-reperfusion injury. 2696 42

Improving the protection of marginal liver grafts during static cold storage is a major hurdle to increase the donor pool of organs. The endothelium glycocalyx quality of preservation influences future inflammatory and oxidative responses. One cellular pathway responsible for the formation of nitric oxide by endothelial cells is dependent on the stimulation of proteoglycans present in the glycocalyx. We investigated the impact of the glycocalyx preservation in static cold storage of fatty liver preserved in different preservation solutions on the endothelium-mediated production of NO. Zucker fatty rat livers were preserved 24 h in static cold storage in either Institut Georges Lopez-1 (IGL-1) (n = 10), IGL-0 (i.e., without PEG35) (n = 5) or Histidine-Tryptophan-Ketoglutarate (HTK) (n = 10) preservation solutions before being processed for analysis. For Sham group (n = 5), the fatty livers were immediately analyzed after procurement. The level of transaminases and nitrites/nitrates were measured in the washing perfusate. Glycocalyx proteins expressions, Syndecan-1, glypican-1 and heparan sulfate (HS), were determined in the tissue (ELISA). Steatotic livers preserved 24 h in IGL-1 preservation solution have a significant lower level of transaminases (aspartate aminotransferase (AST), alanine aminotransferase (ALT)) and less histological damages than steatotic livers preserved 24 h with HTK (p = 0.0152). The syndecan-1 is significantly better preserved in IGL-1 group compared to HTK (p < 0.0001) and we observed the same tendency compared to IGL-0. No significant differences were observed with glypican-1. HS expression in HTK group was significantly higher compared to the three other groups. HS level in IGL-1 was even lower than IGL-0 (p = 0.0005) which was similar to Sham group. The better protection of the glycocalyx proteins in IGL-1 group was correlated with a higher production of NO than HTK (p = 0.0055) or IGL-0 (p = 0.0433). IGL-1 protective mechanisms through the formation of NO could be due to its better protective effects on the glycocalyx during SCS compared to other preservation solutions. This beneficial effect could involve the preservation state of syndecan-1 and the internalization of HS.
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PMID:Glycocalyx Preservation and NO Production in Fatty Livers-The Protective Role of High Molecular Polyethylene Glycol in Cold Ischemia Injury. 3010 65

Sigma-1 receptor (Sig-1R) is a ligand-operated protein that modulates activity of various proteins. It is expressed within the endoplasmic reticulum membranes of multiple organs. We examined the role of Sig-1R in hepatic ischemia-reperfusion injury (IRI). We studied IRI indicators in Sig-1R-/- mice and compared them with wild-type controls. In addition, we assessed the influence of Sig-1R agonist, fluvoxamine, on IRI in both types of animals. We found that Sig-1R-/- mice exhibited significantly decreased liver damage after hepatic IRI as compared to wild-type mice. This effect was manifested by decreased serum levels of alanine aminotransferase (AST), aspartate aminotransferase (ALT), myeloperoxidase (MPO), and supernatant level of lactate dehydrogenase (LDH), decreased endothelial glycocalyx shedding indexed by decreased serum levels of heparan sulfate and syndecan-1, slightly improved liver histology and reduced metalloproteinase-9 expression. Furthermore, in comparison to Sig-1R-/- mice, fluvoxamine significantly increased serum levels of AST, ALT, MPO, and LDH in wildtype animals in a dose-dependent manner at 6 h after IRI. Our findings demonstrate that the absence of Sig-1R provides a protective effect during hepatic IRI. Sig-1R-mediated signaling pathways may play distinct roles in IRI in different organs. The dynamic interaction between Sig-1R and other signaling molecules in different organs needs to be examined further.
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PMID:The role of Sigma-1 receptor agonist in hepatic ischemiareperfusion injury. 3266 Jan 97