Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.26 (invertase)
 4,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the present study, we aimed to protect the intestinal mucosa from small bowel damage in methotrexate (MTX)-treated rats. The protective effect of prostaglandin E2 (PGE2) was investigated. Ileal integrity was evaluated making use of different biochemical parameters: content of sucrase and maltase activities, contents of DNA, proteins, AMPc, PGE2, putrescine (Put), spermine (Spm) and spermidine (Spd). Rats were orally administered 0.5 ml of NaCl solution (0.9%) containing or not containing 400 micrograms.ml-1 of PGE2 twice daily, during three or ten days. Half an hour after the 18th ingestion of PGE2, 0.5 ml of NaCl solution (0.9%) containing MTX (16 mg.ml-1) was injected intravenously. Rats were killed exactly 48 hours after this injection. MTX had no effect on the Put content, increased the AMPc content and decreased the contents of DNA, proteins, Spm, Spd, PGE2 and sucrase or maltase activity. PGE2 had no effect on the biochemical parameters we studied, except on the contents of DNA (10-day treatment) and of PGE2 (3- and 10-day treatment). When MTX was injected after PGE2 treatment, as compared with what was observed when MTX was used as reported above, we observed--an increase in spermine content after 3-day PGE2 treatment and- an increase in the contents of DNA, Spm, Spd and disaccharidase activity after 10-day PGE2 treatment. No other significant variation in the other biochemical parameters was recorded, whatever the duration of the PGE2 treatment. These results indicate that PGE2 could partially protect the intestinal mucosa against the biochemical effects of MTX. Other experimental conditions may need to be chosen in order to obtain a better cytoprotective effect of PGE.
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PMID:Effect of methotrexate on the intestinal mucosa of PGE2-treated rats. 255 77

High doses of 16,16-dimethyl prostaglandin E2 (dmPGE) are trophic to the small bowel of adult and suckling rats. In suckling rats this effect is paralleled by an increase in brush border enzyme activities, possibly indicating accelerated mucosal maturation. To investigate the possible physiological significance of this phenomenon, we examined whether this induction of intestinal enzyme activities can be reproduced in adult rats and whether cell growth and enzyme activity might be suppressed by indomethacin. Treatment twice daily for 2 weeks with 100 micrograms/kg dmPGE by intragastric instillation increased villus length in the proximal and distal small bowel by 36% and 40%, respectively, while 2 mg/kg indomethacin by subcutaneous injection had no effect. Maltase, trehalase, lactase, and sucrase activities were unchanged after dmPGE or indomethacin. [3H]-thymidine incorporation into DNA was not significantly influenced for up to 24 h after a single dose of both 100 micrograms/kg PGE intragastrically or 10 mg/kg indomethacin subcutaneously. These studies confirm that in adult rats large doses of 16,16-dm PGE2 increase the volume of the small-bowel mucosa. In contrast to the situation in suckling rats, the activity of hydrolytic brush border enzymes is not increased. There is thus no evidence that endogenous prostaglandins are trophic or influence brush border enzymes in the adult rat.
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PMID:Influence of 16,16-dimethyl prostaglandin E2 on morphology and brush border enzymes of small-bowel mucosa. Differences in reactivity between adult and suckling rats. 392 42