Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Liver regeneration after omeprazole (OMP) or famotidine (FAM) administration was examined in 66% hepatectomized rats. The regeneration was evaluated by the liver weight as a percentage of body weight (LRR) and the proportion of hepatocytes in mitosis per 1,000 counts (MI). Administration of OMP 0.4 mg/kg per day for 3 or 7 days suppressed LRR and MI 3 and 7 days after hepatectomy. However, the administration of FAM 0.8 mg/kg per day for 3 or 7 days did not change either LRR or MI. Increased gastrin levels in the blood were seen only after OMP administration. The food intake was unchanged by OMP or FAM, but FAM increased water intake. The liver functional score, glutamic pyruvic transaminase and alkaline phosphatase in the blood all increased with OMP, but FAM had no apparent effect on the hepatic or renal function. These observations suggest that a large dosage of OMP suppresses liver regeneration, while FAM appears to have no meaningful effect on regeneration.
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PMID:The liver regenerative response elicited by antisecretory agents in partially hepatectomized rats: a comparison between omeprazole and famotidine. 855 1

Liver regeneration after injury with carbon tetrachloride (CCl4) followed by partial hepatectomy is a complex model involving toxicological, inflammatory, and necrotic processes. In the present study, the time-course of hepatic regenerative process was investigated in relation to hepatic stimulator substance (HSS) activity, administration of a single dose of CCl4 and partial (70%) hepatectomy in male rats. To evaluate liver injury events, the levels of serum aspartic aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) were measured. Hepatic DNA synthesis reached a maximum at 36 hr after hepatectomy in contrast to the reported 24-hr and 32-hr peaks observed in nontreated hepatectomized rats. On the other hand, HSS activity appeared to peak at 28, 40, and 44 hr after hepatectomy in CCl4-treated rats, and it was quite a lot lower at 24, 32, 36, 48, and 60 hr. The hypothesis that HSS promotes liver regeneration but it does not initiate it, as other factors have been found to do, is discussed.
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PMID:Levels of hepatic stimulator substance in liver regenerating process of partially hepatectomized rats pretreated with a single dose of carbon tetrachloride. 1023 17

Hepsin, a liver-enriched novel serine protease, has been implicated in participating with normal cell growth, embryogenesis, and blood coagulation pathway. To study its function in vivo, we have disrupted the mouse hepsin gene by homologous recombination. Targeted disruption of the hepsin gene and ablation of hepsin message were demonstrated by Southern blotting, Northern blotting and RT-PCR analysis. Homozygous hepsin -/- mice were viable, fertile, and exhibited no gross abnormalities, as judged by the size, weight and blood coagulation (PT) assays. However, the serum concentration of the bone form of alkaline phosphatase, aspartate aminotransferase, and alanine aminotransferase of the hepsin -/- mice was mildly elevated, in spite of no obvious pathological change of hepatocytes. To examine whether hepsin is involved in controlling cell growth in adult tissues, 70% hepatectomy was applied to the hepsin -/- mice. Liver regeneration proceeded normally in the hepsin -/- mice as judged by the liver mass restoration rate. These results suggest that loss of hepsin function causes no effect in cell growth and embryogenesis in vivo, which is in contradiction to the studies using in vitro cell culturing system. Moreover, gross mass regeneration of liver after damage proceeds normally in the absence of functional hepsin.
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PMID:Mice deficient in hepsin, a serine protease, exhibit normal embryogenesis and unchanged hepatocyte regeneration ability. 1112 69

Acetaminophen (APAP) is a widely-used analgesic and a known hepatotoxic agent. Vascular endothelial growth factor (VEGF) is a growth factor with multiple functional roles. VEGF plays an important role in angiogenesis and hepatic regeneration. The aim of this study was to determine the expression of VEGF isoforms and its receptors throughout liver regeneration after the administration of a toxic dose of APAP in rats. Ten groups of adult male rats received a dose of 3.5 g/kg b.w. of APAP per os. The rats were killed post administration at 0-288 h. Blood and liver tissue were extracted. Determination of serum transaminases and alkaline phosphatase activities was performed. Liver injury and regeneration were assessed with hematoxylin-eosin specimens, morphometric analysis, hepatic thymidine kinase assay and Ki-67 expression. Reverse transcription-polymerase chain reaction and immunohistochemical methods were used for assessment of VEGF isoforms and receptors differential expression. High activities of aspartate aminotransferase were observed at 24 and 36 h with another peak of activity at 192 h post administration. Alanine aminotransferase was highest at 36 h. Alkaline phosphatase was increased post 24 h being higher at 72,192 and 240 h. Centrilobular necrosis was observed at 48-72 h and thorough restoration of the liver microarchitecture was observed at 288 h. Liver regeneration lasted from 24-192 h according to the results from thymidine kinase activity and Ki-67 expression. VEGF and VEGF receptor-2 m-RNA levels presented with a three-peak pattern of expression at 12-24, 72-96 and 192-240 h post administration. Significant difference was noted between periportal and centrilobular immunohistochemical expression. VEGF proves to play a critical role during APAP-induced liver regeneration as it presents with three points of higher expression. The first two time points are associated with the initial inflammatory reaction to the noxious stimulus and the hepatocyte regenerative process where as the third one is indicative of the potential involvement of VEGF in processes of remodeling.
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PMID:VEGF isoforms and receptors expression throughout acute acetaminophen-induced liver injury and regeneration. 1743 90