Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.1 (aspartate aminotransferase)
 21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The reported cytoprotective effects of prostaglandins against noxious stimuli in the liver was the basis for the present investigations of the effects of prostacyclin (PGI2) and a prostaglandin analogue (BW 245C) in an animal model of severe liver failure. Rats were given galactosamine at two dose levels and the prostaglandins were given in repeated doses from 0 to 6 h during the development of the liver damage or in another group from 24 to 30 h at the time of maximal liver injury. For PGI2 significant cytoprotection was found as assessed by a reduction in blood Normotest at 24, 48 and 72 h (P less than 0.05) and the plasma level of aspartate aminotransferase at 24 and 48 h (P less than 0.02) and the lysosomal markers N-acetyl-beta-glucosaminidase at 24, 48 and 72 h (P less than 0.001) and cathepsin D at 48 h (P less than 0.005) as compared to appropriate controls. Early administration of PGI2 reduced the mortality rate from 63% in the control group to 0% (P less than 0.01) in the treated group, but no significant effects were found when either compound was given later in the 24-h to 30-h period.
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PMID:Effect of prostacyclin (PGI2) and a prostaglandin analogue BW 245C on galactosamine-induced hepatic necrosis. 351 86

The activities of the lysosomal enzymes acid and neutral protease, N-acetylglucosaminidase, and acid phosphatase were measured in the serum of patients with fulminant hepatic failure. Acid protease (cathepsin D) activity was increased about tenfold in patients who died and nearly fourfold in those who survived fulminant hepatic failure after paracetamol overdose, whereas activities were increased equally in patients with fulminant hepatic failure due to viral hepatitis whether or not they survived. A correlation was found between serum acid protease activity and prothrombin time, and the increase in cathepsin D activity was sustained over several days compared with aspartate aminotransferase, which showed a sharp early peak and then a fall. Circulating lysosomal proteases can damage other organs, and measurement of their activity may therefore be of added value in assessing prognosis in this condition.
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PMID:Circulating lysosomal enzymes and acute hepatic necrosis. 700 43

Baicalein has been proved as a promising compound for non-alcoholic fatty liver disease (NAFLD); however, the molecular mechanisms underlying the progression of NAFLD and its intervention by baicalein remain largely obscure. Male C57BL/6J fed high-fat diet (HFD) and HepG2 cells stimulated with free fatty acid were treated with baicalein and various pharmacological reagents to explore the effect of signaling pathways involved in lysosomal acidification. Baicalein intake declined ALT and AST activities by 25.1% and 18.7%, respectively, compared with the HFD group. Moreover, baicalein markedly ameliorated the HFD-trigged lysosomal membrane permeabilization evidenced by declined cathepsin B release. Subsequent disorders, including cathepsin D maturation and mitochondrion membrane potential were also partially normalized by baicalein administration to HFD-fed mice. Meanwhile, an increase in V-ATPase V1 subunits expression in lysosomes, V-ATPase activity and the colocalization of cytosol V-ATPase V1 subunits and lysosomes was observed in baicalein-supplement mice. Bafilomycin A1 stimulation resulting in elevated lysosomal pH and triacylglycerol accumulation partially abolished the effect of baicalein. Furthermore, incubation with mTOR inhibitor rapamycin restored lysosomal pH and decreased cellular triacylglycerol content. Collectively, these findings demonstrate that hepatic lysosomal acidification is the main target of baicalein against NAFLD via maintaining lysosomal V-ATPase assembly through mTOR pathway.
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PMID:Baicalein attenuates impairment of hepatic lysosomal acidification induced by high fat diet via maintaining V-ATPase assembly. 3175 65