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)

Silymarin has been claimed to have a benificial effect in various types of liver injury. In a prospective study in patients with acute viral hepatitis (n = 151) the effectiveness of this drug on the cause of the disease was tested. The groups with and without Silymarin (Legalon) were comparable concerning age and sex distribution and the frequency of HBs-antigen positive hepatitis; Laboratory findings (total serum bilirubin, activity of GOT, GPT and alkaline phosphatase and prothrombin time) were determined in intervals of 5 to 7 days over a period of 5 weeks beginning with the onset of jaundice. There were no statistical significant differences between both groups in the decrease of mean values of all parameters tested. The frequency of nearly normalized values of transaminases and serum bilirubin after 10, 20 and 30 days was not higher in the group treated with Silymarin as compared to the controls. It is concluded that Silymarin has no favourable effects on the cause of acute viral hepatitis.
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PMID:[Silymarin for the treatment of acute viral hepatitis? Report of a controlled trial (author's transl)]. 84 Jan 25

The effect of silymarin on liver lipid peroxidation and membrane lipid alterations induced by an acute dose of CCl4 was studied. Four groups of animals were treated with CCl4, CCl4 + silymarin, silymarin and its vehicles. CCl4 was given orally (0.4 g 100 g-1 body wt.) and silymarin was administered i.p. All animals were sacrificed 24 h after the treatments. Liver lipid peroxidation was measured and plasma membranes were isolated. Alkaline phosphatase (AP) and gamma-glutamyl transpeptidase (GGTP) were measured in plasma membranes. Membrane lipids were extracted and then analysed by thin-layer chromatography by measuring the phosphorus of the phospholipids in each spot. Liver lipid peroxidation was increased about three times in the group receiving CCl4 only. Silymarin cotreatment prevented this increase. Phosphatidylethanolamine (PEA) decreased, while phosphatidylinositol (PI) increased in the plasma membranes isolated from the CCl4-treated group. Animals that received CCl4 + silymarin showed no decrease in PEA content. A partial prevention of the decrease in phosphatidylinositol content was also observed in plasma membranes of animals treated with silymarin in addition to CCl4. CCl4 decreased gamma-glutamyl transpeptidase (GGTP) and alkaline phosphatase (AP) membrane activities. Silymarin cotreatment prevented the AP (completely) and the GGTP (partially) falls caused by CCl4. Silymarin by itself increased AP membrane activity. A significant relationship between the membrane content of phosphatidylethanolamine (PEA) and the AP activity was observed in plasma membranes of treated animals and in normal liver membranes enriched with PEA. These results indicate that silymarin can protect against the alterations induced by CCl4 on the liver plasma membrane through its antioxidant properties by modifying the plasma membrane phospholipid content.
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PMID:Prevention by silymarin of membrane alterations in acute CCl4 liver damage. 197 58

The efficacy of silymarin treatment in preventing biochemical and histological alterations in CCL4-induced liver cirrhosis in rats was studied. Four groups of rats were treated with: (1) CCL4; (2) mineral oil; (3) CCL4 + silymarin; and (4) silymarin. All animals were sacrificed 72 h after the end of treatments. The activities of alkaline phosphatase (alk. phosp.), gamma-glutamyl transpeptidase (GGTP), glutamic pyruvic transaminase (GPT) and glucose-6-phosphatase (G6Pase), and bilirubin content were determined in serum. Na+, K+-ATPase and Ca++-ATPase activities were measured in isolated plasma membranes. Lipoperoxidation, triglycerides (TG), and glycogen contents were also measured in liver homogenates. Liver cirrhosis was evidenced by significant increases in liver collagen, lipoperoxidation, serum activities of alk. phosp., GGTP, GPT, G6Pase, bilirubin content, and liver TG. Activities of ATPases determined in plasma membranes were significantly reduced, as was liver glycogen content. Silymarin cotreatment (50 mg/kg b.wt) completely prevented all the changes observed in CCL4-cirrhotic rats, except for liver collagen content which was reduced only 30% as compared to CCL4-cirrhotic rats. Silymarin protection can be attributed to the agent's antioxidant and membrane-stabilizing actions.
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PMID:Prevention of CCL4-induced liver cirrhosis by silymarin. 254 40

Silymarin, a flavolignan from the seeds of Silybum marianum, showed significant hepatoprotective activity in P. berghei-induced hepatic damage in M. natalensis, as assessed by changes in several serum and liver biochemical parameters. Changes in lipoprotein-X, GOT, GPT, alkaline phosphatase and bilirubin were found to be protected by silymarin at different doses. Maximum activity was observed at a dose of 5 mg/kg bw, po. Silymarin had no effect on parasitaemia.
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PMID:Hepatoprotective activity of silymarin against hepatic damage in Mastomys natalensis infected with Plasmodium berghei. 269 91

The effect of silymarin (100 mg/kg i.p.) on the biochemical indicators of liver damage induced by thallium (10 mg/kg p.o.) was studied in rats. The production of malondialdehyde and the content of reduced glutathione in the liver were measured as indicators of lipid peroxidation. Thallium intoxication increased the serum activities of glutamic pyruvic transaminase, gamma-glutamyl transpeptidase, alkaline phosphatase and the liver concentration of triglycerides. Thallium decreased the activity of alkaline phosphatase and increased that of gamma-glutamyl transpeptidase in the liver cell membrane. It also abolished the membrane activity of Na+/K+ ATPase. Lipid peroxidation was enhanced by thallium as malondialdehyde production was increased and the content of reduced glutathione was decreased in the liver. Silymarin completely prevented all these changes. It is suggested that thallium toxicity is due, at least in part, to the promotion of lipid peroxidation. The membrane stabilizing effect of silymarin observed in this and in other models of liver toxicity is due to some antioxidant property, possibly related to its ability to scavenge free oxygen radicals.
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PMID:Protection against thallium hepatotoxicity by silymarin. 323 Feb 45

A single oral dose of the lyophilized deathcap fungus Amanita phalloides (85 mg/kg body wt) caused gastrointestinal signs of diarrhea, retching, and vomiting in beagles after a latent period of 16 hr. The pathologic lesions; the increases in serum transaminase (GOT, GPT), alkaline phosphatase, and bilirubin, as well as the fall in prothrombin time all indicated that liver damage was maximal at about 48 hr after poisoning. Four of twelve dogs given A. phalloides died with signs of hepatic coma within 35 to 54 hr with the biochemical values in the survivors reverting to normal by the ninth day. Silibinin administration (50 mg/kg) 5 and 24 hr after intoxication suppressed the serum changes and the fall in prothrombin time. The degree of hemorrhagic necrosis in the liver was markedly reduced, and none of the silibinin-treated dogs died.
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PMID:Protection by silibinin against Amanita phalloides intoxication in beagles. 671 56

Silymarin (SIL), a standardized plant extract containing about 60% polyphenole silibinin, is used as a hepatoprotective agent. Its antifibrotic potential in chronic liver diseases has not been explored. Therefore, we applied SIL to adult Wistar rats that were subjected to complete bile duct occlusion (BDO) by injection of sodium amidotrizoate (Ethibloc). This treatment induces progressive portal fibrosis without significant inflammation. Rats with sham-operation that received SIL at 50 mg/kg/d (n = 10) and rats with BDO alone (n = 20) served as controls, whereas groups of 20 animals were fed SIL at a dose of 25 and 50 mg/kg/d during weeks 1 through 6 or doses of 50 mg/kg/d during weeks 4 through 6 of BDO. Animals were sacrificed after 6 weeks for determination of blood chemistries, total and relative liver collagen (as hydroxyproline [HYP]), and the serum aminoterminal propeptide of procollagen type III (PIIINP). BDO in untreated rats caused an almost ninefold increase in total liver collagen (16.1 +/- 3.1 vs. 1.8 +/- 0.4 mg HYP, P < .001). SIL at 50 mg/kg/d reduced total HYP by 30% to 35%, either when given from week 1 through 6 or from week 4 through 6 after BDO (10.6 +/- 2.7 and 10.2 +/- 3.9 mg HYP, both P < .01 vs. BDO alone), whereas 25 mg/kg/d were ineffective. Because SIL at 50 mg/kg/d also reduced the collagen content per gram of liver tissue, it acted as a true antifibrotic agent. The single value of PIIINP at killing paralleled the antifibrotic activity of SIL with 11.6 +/- 3.8 and 9.9 +/- 3.7 vs. 15.3 +/- 5.2 microg/L in both high-dose groups (P < .05 and P < .01, respectively, vs. rats with BDO alone). Except for a decreased alkaline phosphatase and a lower histological fibrosis score in the groups that received SIL, clinical-chemical parameters were not different among all groups with BDO. We therefore conclude that 1) BDO with Ethibloc is a suitable model to test for pure antifibrotic drugs because it induces progressive rat secondary biliary fibrosis without major inflammation; 2) oral SIL can ameliorate hepatic collagen accumulation even in advanced (biliary) fibrosis; and 3) PIIINP appears to be a suitable serum marker to monitor the inhibition of hepatic fibrogenesis in this model of biliary fibrosis.
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PMID:Silymarin retards collagen accumulation in early and advanced biliary fibrosis secondary to complete bile duct obliteration in rats. 1117 60

Ursodeoxycholic acid (UDCA) is a safe and effective medical therapy for most patients with primary biliary cirrhosis (PBC), but some patients show an incomplete response. Silymarin is a potent antioxidant with immunomodulatory and antifibrotic properties. The aim of this study was to evaluate the safety and assess the efficacy of silymarin in patients with PBC who had shown a suboptimal response to UDCA. Twenty-seven patients with PBC who had been on UDCA (13-15 mg/kg/day) therapy for 7 to 221 months and had shown a persistent elevation of alkaline phosphatase activity at least 2 times the upper limit of normal for more than 6 months were enrolled. Oral silymarin, 140 mg 3 times daily was given for 1 year, and patients continued on the same dosage of UDCA. No significant changes in serum alkaline phosphatase activity (897 +/- 84 vs. 876 +/- 95, P =.5), total bilirubin (0.9 +/- 0.1 vs. 1 +/- 0.1, P =.07), aspartate transaminase (AST) (58 +/- 5 vs. 56 +/- 6, P =.4), albumin (4.0 +/-.06 vs. 4.1 +/-.06, P =.4), or Mayo risk score (3.82 +/- 0.2 vs. 3.88 +/- 0.2, P =.4) were noted after 1 year of treatment with combination therapy. Transitory gastrointestinal adverse events occurred in 2 patients. In conclusion, although silymarin was well tolerated, this medication did not provide benefit to patients with PBC responding suboptimally to UDCA. The results of this pilot study would seem to discourage further controlled trials of silymarin in patients with PBC.
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PMID:Silymarin in the treatment of patients with primary biliary cirrhosis with a suboptimal response to ursodeoxycholic acid. 1117 60

R. tomentosus is a vegetal species closely related to the culinary rosemary (R. officinalis), a plant reported to contain antihepatotoxic agents. A dried ethanol extract of the aerial parts of Rosmarinus tomentosus (Lamiaceae) and its major fraction separated by column chromatography (fraction F19) were evaluated for antihepatotoxic activity in rats with acute liver damage induced by a single oral dose of thioacetamide. Silymarin was used as a reference antihepatotoxic substance. Pre-treatment with R. tomentosus ethanol extract, fraction F19 or silymarin significantly reduced the impact of thioacetamide toxicity on plasma protein and urea levels as well as on plasma aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase and gamma-glutamyl transpeptidase activities compared with thioacetamide-treated animals (group T). Pre-treatment with R. tomentosus ethanol extract significantly reduced the impact of thioacetamide damage on alkaline phosphatase and gamma-glutamyl transpeptidase activities compared with group T. Silymarin administration significantly reduced alkaline phosphatase and gamma-glutamyl transpeptidase activities compared with group T. Fraction F19 administration reduced only alkaline phosphatase activity compared with group T. According to these data, R. tomentosus extract shows promising antihepatotoxic activity, suggesting the need to isolate the chemical principles responsible for this activity and to study this activity in a model of thioacetamide-induced cirrhosis.
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PMID:Antihepatotoxic activity of Rosmarinus tomentosus in a model of acute hepatic damage induced by thioacetamide. 1105 42

The different extracts of the fruits of Luffa echinata Roxb. (Cucurbitaceae) were tested for their hepatoprotective activity against CCl(4) induced hepatotoxicity in albino rats. The degree of protection was measured by using biochemical parameters like serum glutamic oxalacetic transaminase (SGOT), serum glutamic pyruvate transaminase (SGPT), alkaline phosphatase (ALKP), total protein (TP) and total albumin (TA). The petroleum ether, acetone and methanolic extracts showed a significant hepatoprotective activity comparable with those of Silymarin.
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PMID:Hepatoprotective activity of Luffa echinata fruits. 1139 Jan 35


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