Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the effect of bicyclol on lipid disorder and liver damage induced by tetracycline in mice, mice were given (ig) bicyclol (75, 150, and 300 mg x kg(-1)) three times before or after administration of tetracycline (180 mg x kg(-1)). The contents of hepatic lipids, MDA and GSH, serum lipids and ALT/AST levels were measured 24 hours after the injection (ip) of tetracycline. The beta-oxidation rate of hepatic mitochondrial fatty acid and hepatic secretion of VLDL were also observed. Bicyclol (150 and 300 mg x kg(-1)) provided significant protection against fatty liver by inhibiting the elevation of hepatic TG and CHO, adjusting abnormal serum lipids, inhibiting the elevation of serum ALT, AST, and ameliorating the severity of pathological changes. Furthermore, bicyclol significantly accelerated the VLDL (TG) secretion and reversed the impairment of mitochondrial oxidation, resulting in the lipid homeostasis. The increase of MDA formation and depletion of GSH that reflect lipid peroxidation induced by tetracycline were also inhibited by bicyclol administration. The results indicated that the hepatoprotection of bicyclol was mostly due to the improvement on lipid oxidation and transportation as well as the inhibition of lipid peroxidation in tetracycline-intoxicated mice.
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PMID:[Protective effect of bicyclol against acute fatty liver induced by tetracycline in mice]. 1835 27

Ganoderma lucidum (GL), a traditional Chinese medicinal mushroom, has been widely used for the treatment of chronic hepatopathy of various etiologies. The hepatoprotective activity of peptides from Ganoderma lucidum (GLP) was evaluated against d-galactosamine (d-GalN)-induced hepatic injury in mice. GLP was administered via gavage daily for 2 weeks at doses of 60, 120 and 180 mg/kg, respectively. Control groups were given the same amount of physiological saline synchronously. Then the mice from d-GalN control and GLP-treated groups were treated with d-GalN (750 mg/kg) suspended in normal saline by intraperitoneal injection. d-GalN-induced hepatic damage was manifested by a significant increase in the activities of marker enzymes (AST, ALT) in serum and MDA level in liver (P<0.01), and by a significant decrease in activity of SOD and GSH level in liver (P<0.01). Pretreatment of mice with GLP reversed these altered parameters to normal values. The biochemical results were supplemented by histopathological examination of liver sections. The best hepatoprotective effects of GLP were observed after treatment with the dose of 180 mg/kg as it was evidenced from biochemical parameters and liver histopathological characters which were similar to those of normal control group. Results of this study revealed that GLP could afford a significant protection in the alleviation of d-GalN-induced hepatocellular injury.
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PMID:Hepatoprotective effects of Ganoderma lucidum peptides against D-galactosamine-induced liver injury in mice. 1840 49

Pringle described a new technique to reduce blood loss during liver surgery. Adult Wistar rats were subjected to 1 h of partial liver ischemia and followed by 3 h reperfusion. Eighteen Wistar rats were divided into sham-operated control group (I) (n=6), ischemia and reperfusion (I/R) group (II) (n=6), L-arginine treated group (100 mg/kg body weight/daily by oral route for 7 d before induced ischemia reperfusion maneuver) (III) (n=6). Ischemic and reperfusion hepatocellular injury occurred as indicated by increased-alanine transaminase (ALT), aspartate transaminase (AST). Pre-treatment with L-arginine significantly decreased serum-ALT, AST after 1 h ischemia followed by 3 h of reperfusion. Nitric oxide production, in hepatocytes was increased 2 fold and MDA levels significantly decreased by L-arginine treatment as compared to I/R rat. Histopathology and TEM studies showed markedly diminished hepatocellular injury in L-arginine pretreated rats during the hepatic I/R, which reached a level comparable to saline-treated rat of sham operated group. Thus, findings it may be concluded that L-arginine afforded significant protection from hepatobiliary function from I/R injury by nitric oxide production.
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PMID:L-arginine protects from pringle manoeuvere of ischemia-reperfusion induced liver injury. 1845 13

Cyclosporine A (CyA) leads to liver injury, probably by causing the production of free radicals and resulting in nitric oxide (NO) deficiency. We evaluated CyA-mediated liver damage histopathologically to determine the possible beneficial effects of L-arginine (L-Arg). In this study, 7 groups of Sprague-Dawley rats; (1) Control group; (2) 0.9% NaCl group; (3) CyA group: 7.5mg/kg/day; (4) L-Arg group: 2g/lt/day; (5) l-NAME (N-nitro-L-arginine methyl ester) group: 5mg/100ml/day; (6) CyA+L-Arg group: L-Arg (2g/lt/day)+CyA (7.5mg/kg/day); and (7) CyA+L-NAME group: CyA (7.5mg/kg/day)+L-NAME (5mg/100ml/day) were included. At the end of the treatments, animals were killed and hepatic tissues were treated for morphological (hematoxylin and eosin) and biochemical (NO and malondialdehyde, MDA) analyses, and serum was processed for biochemical (alanine transaminase (ALT), aspartate transaminase (AST), bilirubin, alkaline phosphatase (ALP) and total protein) study. The results indicated that CyA-induced hepatotoxicity was characterized by sinusoidal dilatation, hepatocellular vacuolization, neutrophilic infiltration and hepatocellular necrosis. These findings were less pronounced in the CyA+L-Arg group than CyA alone group. L-NAME group showed moderate changes. The CyA+L-NAME (Group 7) had more severe changes. We found changes in tissue NO and MDA levels. We think that the tissue damage caused by CyA is mild and reversible at the period when biochemical parameters are just starting to become abnormal and that L-Arg may have a protective effect against CyA damage on liver.
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PMID:Oral L-arginine protects against cyclosporine-induced hepatotoxicity in rats. 1858 16

Sepsis is still a major cause of the high mortality rate in the intensive care unit. Many studies have been published about the severity of sepsis, but the cause of mortality in sepsis and multiorgan failure is still obscure. This study investigated the effects of caffeic acid phenethyl ester (CAPE) particularly on the inflammatory and related histopathological changes in the lung, liver and kidney in an experimental sepsis model. Forty Sprague Dawley rats were used in this study, and were divided into four groups of ten rats each, as follows: Group I was given intraperitoneal saline infusion treatment. Group II was given intraperitoneal CAPE infusion treatment. Sepsis was induced in the animals in Group III (sepsis with saline infusion), while Group IV rats underwent induced sepsis plus CAPE infusion treatment (sepsis with CAPE infusion). Sampling was performed 48 h after treatment. The induction of sepsis resulted in a significant increase in serum glucose, leukocytes, urea, creatinine, LDH levels in BAL, plasma MDA, AST and ALT levels in the sepsis + saline group. The use of CAPE significantly decreased these parameters. Histopathological examination revealed less congestion, portal inflammation, and focal necrosis of the liver, and less congestion, edema, and emphysematous and inflammatory changes in the lung in the sepsis + CAPE group than in the other groups. These results support that CAPE may be used for the treatment of organ failure during sepsis.
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PMID:Effects of caffeic acid phenethyl ester (CAPE) on sepsis in rats. 1860 6

The present study was undertaken to investigate the protective effect of royal jelly against paracetamol-induced liver damage. The study was conducted in 90 female Swiss Albino mice, and six groups were established. While the first group was maintained as control, Groups 2-6 were administered 200mg/kg RJ for 1 day, 200mg/kg RJ for 7 days, 400mg/kg PAR for 1 day, 200mg/kg RJ plus 400mg/kg PAR for 1 day and 200mg/kg RJ for 7 days and then second 400mg/kg PAR on the 7th day, orally, respectively. It was shown that PAR significantly increased serum ALT, AST, ALP, liver MDA levels and significantly decreased liver GSH-Px activity, when compared to the control group (Group 1). On the other hand, meaningful changes were observed in the biochemical parameters of the group which was administered long-term RJ (Group 6). The aforementioned parameters which were statistically significant were determined to have drawn closer to values of the control group, and among these, the existing statistical differences for MDA level and GSH-Px activity between the trial group (Group 6) and the control group disappeared (Group 1). Compared to the pathological changes observed in the liver parenchyma, remark cords, sinusoids and hepatocytes in the group which was administered paracetamol alone (Group 4), lesions were determined to be less severe particularly in the group (Group 6) which received royal jelly for 7 days prior to paracetamol. In conclusion, the administration of royal jelly as a hepatoprotective agent for 7 days against paracetamol-induced liver damage was determined to exhibit marked protective effect on liver tissue.
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PMID:The effects of royal jelly on liver damage induced by paracetamol in mice. 1869 95

In this study, 28 Wistar female rats (200-250g) were used and divided into four equal groups. Group 1 was allocated as the control group. Groups 2-4 were administered 100mg/kg/bw/day bee pollen, 20mg/kg/bw/day propoxur, and 100mg/kg/bw/day bee pollen plus 20mg/kg/bw/day propoxur by gavage for 14 days, respectively. At the end of the 14th day, blood and tissues (the liver, kidney, brain, and heart) were collected from all animals. Oxidative stress markers (MDA, CAT, SOD, GSH-Px) and some other biochemical parameters (total protein, albumin, glucose, cholesterol, triglyceride, BUN, creatinine, uric acid, magnesium, sodium, potassium, chloride, total bilirubin, GGT, LDH, AST, ALT, and ALP) were analyzed. According to the data obtained, propoxur was determined to lead to negative changes in most of the biochemical parameters investigated and the administration of bee pollen was determined to alleviate these effects.
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PMID:Evaluation of protective effect of bee pollen against propoxur toxicity in rat. 1870 57

The protective effects of diallyl trisulfide (DATS) on acute ethanol-induced liver injury were investigated. Mice were pretreated with DATS (30mg/kgbw) for 7d before being exposed to ethanol (4.8g/kgbw). The biochemical indices (aspartate amino transferase, AST; alanine amino transferase, ALT; triglyceride, TG) were examined to evaluate the protective effects. Mitochondria were isolated for the mitochondrial permeability transition (MPT), membrane potential (DeltaPsi(m)) and adenosine nucleotide pool assay. The lipid peroxidation (malondialdehyde, MDA), non-enzymatic antioxidant (glutathione, GSH) and enzymatic antioxidants (superoxide dismutase, SOD; catalase, CAT; glutathione reductase, GR; glutathione peroxidase, GSH-Px) were measured both in the liver homogenate and isolated mitochondria. Acute ethanol exposure resulted in the significant increase of the ALT, AST and TG levels and hepatic mitochondria dysfunction shown as MPT, and the decreases of DeltaPsi(m), ATP and energy charge (EC). However, DATS pretreatment dramatically attenuated these adverse effects. Beside this, DATS was found to significantly inhibit the increase of the hepatic and mitochondrial MDA levels, which were decreased by 33.3% (P<0.01) and 39.0% (P<0.01), respectively. In addition, DATS pretreatment markedly suppressed the ethanol-induced decrease of the hepatic GSH level and increased the mitochondrial GSH level. Moreover, the activities of the hepatic antioxidant enzymes (SOD, CAT, and GR) and the mitochondrial antioxidant enzymes (SOD, GR, and GSH-Px) were significantly boosted. Thus, we concluded that DATS dramatically attenuated acute ethanol-induced liver injury and mitochondrial dysfunction. The increase of the hepatic and mitochondrial GSH levels and the elevation of the antioxidant enzymes activities should account for the preventive effects.
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PMID:Diallyl trisulfide (DATS) effectively attenuated oxidative stress-mediated liver injury and hepatic mitochondrial dysfunction in acute ethanol-exposed mice. 1875 35

In this study, 42 female Wistar albino rats, weighing between 200 and 250 g, were used and they were divided into six equal groups. Group 1 was allocated as the control group. Rats included in groups 2 and 3 were administered a water-solubilized extract of bee pollen at a dose of 50 mg/kg bw/day and 100 mg/kg bw/day, respectively. Group 4 received 225 mg/kg bw/day carbaryl. Groups 5 and 6 were given a water-solubilized extract of bee pollen at a dose of 50 mg/kg bw/day and 100mg/kg bw/day, respectively, plus 225 mg/kg bw/day carbaryl. The indicated administrations were continued for 21 days for groups 1-6 by gavage. MDA levels and the activities of CAT, SOD and GSH-Px were analysed in blood and tissues (liver, kidney, brain and heart). At the same time, levels/activities of total protein, albumin, glucose, triglyceride, T-cholesterol, T-bilirubin, BUN, creatinine, uric acid, GGT, LDH, AST, ALT and ALP, magnesium, sodium, potassium and chloride were evaluated in serum samples. In conclusion, carbaryl was determined to cause negative changes in most of the oxidative stress markers and serum biochemical parameters investigated. These effects were observed to alleviate with the administration of bee pollen.
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PMID:Effect of carbaryl on some biochemical changes in rats: the ameliorative effect of bee pollen. 1899 65

This study was designed to investigate the protective and antioxidant properties of Punica granatum (PG) beverage against trichloroacetic acid (TCA)-exposure in rats. The hepatopreventive and antioxidant potential of the plant's infusion was evaluated by measuring level of serum enzymes, antioxidant defense systems (ADS) and lipid peroxidation content in various organs of rats. Three experimental groups: A (untreated=control), B (only TCA-treated) and C (TCA+PG treated). According to the results, while the levels of AST and ALT increased significantly in B groups' they decreased significantly in the C groups'. LDH and CK did not change significantly in B groups' whereas decreased significantly in the C groups'. Liver, brain, kidney and heart tissues MDA content significantly increased in B groups', whereas no significant changes were observed in the C groups'. On the other hand, SOD decreased significantly in liver of the B group but did not change significantly in the C groups'. GST activity increased significantly in liver, brain and spleen of C group while significant decrease was observed for kidney as compared to those of control. Hence, the study reveals that constituents present in PG impart protection against carcinogenic chemical induced oxidative injury that may result in development of cancer during the period of a 52-day protective exposure.
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PMID:Hepatoprotective role and antioxidant capacity of pomegranate (Punica granatum) flowers infusion against trichloroacetic acid-exposed in rats. 1902 27


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