Biomedical subjects
Publications and source records attributed to F Capasso.
The laxation induced by senna is not modified in rats either maintained on a diet deficient in essential fatty acids (EFAD) or exposed to cold (6 degrees C) or with yeast-induced fever. In light of our findings it appears conceivable that non-PG-mediated mechanism(s) play a relevant role in laxation induced by senna.
Thirty-four new N-acylderivatives of 7-amino-2,3-polymethyleneinoles (I) and (II) were prepared and tested, together with a few analogues previously obtained, against carrageenan edema in the rat. Several compounds, at a dose of 1 mmole/kg, exhibit good inhibitory activity, that in some cases is superior to that displayed by indomethacin at a dose of 5 mg/kg. With only one exception, activity is confined to compounds of formula (I) and, generally, derivatives of 2,3-hexamethyleneindole are more active than those of lower homologues.
Intestinal tissues of man, rat, mouse, guinea-pig and rabbit were preincubated with laxatives, homogenised, and incubated with [14C]arachidonic acid. After extraction into chloroform, the eicosanoids were separated by thin layer chromatography. Metabolism of [14C]arachidonic acid into prostaglandins (PGs), and the lipoxygenase products LTB4 and 5-HETE, was stimulated by ricinoleic acid (100 micrograms/ml) or phenolphthalein (100 micrograms/ml), and to a lesser extent by picosulphate (125 micrograms/ml) and sulfosuccinate (200 micrograms/ml). Mannitol (500 micrograms/ml) had no effect. Indomethacin (1 microgram/ml) inhibited the stimulation of PG formation. The dual pathway inhibitor BW755C (1 microgram/ml) reduced the formation of prostaglandins, LTB4 and 5-HETE. In some experiments on rat colon, prostanoids were separated from lipoxygenase products, characterised by their chromatographic mobility and quantitated (relative amounts PGE2 greater than PGF2 alpha greater than TXB2 greater than PGD2). Their formation was enhanced by ricinoleic acid (100 micrograms/ml) and inhibited by either indomethacin or BW 755C (1 microgram/ml). The present results indicate that mammalian isolated gut tissue can convert [14C]arachidonic acid into both cyclo-oxygenase and lipoxygenase products, and support the suggestion that eicosanoids may participate in the laxative effect of some secretagogues.
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1 Cholera toxin injected i.v. into rats stimulated the production of prostaglandin E2 (PGE2), leukotriene B4 (LTB4) and LTC4 by segments of jejunum, but it had no effect when added to the tissue in vitro. 2 Pretreatment of the animals with the compound BW 755C reduced the increased production of PGE2, LTB4 and LTC4 by i.v. cholera toxin. Pretreatment with indomethacin reduced the production of PGE2. 3 These findings are consistent with the hypothesis that arachidonate metabolites are involved in the diarrhoea induced by cholera toxin.
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The effects of some laxatives were examined on the formation of histamine, 5-hydroxytryptamine (5-HT) and prostaglandin-like material (PG-LM) by rat intestine in-vitro. Castor oil, senna, sulphosuccinate and bisacodyl, but not mannitol or lactulose, in doses that cause laxation, increased the formation of histamine, 5-HT and PG-LM. Indomethacin or hydrocortisone reduced the increase of PG-LM formation. The data support the idea that the laxative effects of these intestinal secretagogues are due to increased intestinal production of PG-LM, histamine and 5-HT.
The effect of feverfew (Tanacetum parthenium L., Schultz Bip.) as a whole plant on an aqueous extract equivalent to 20 mg dried plant per ml, has been examined on both cyclo-oxygenase and lipoxygenase activity in rat leucocytes in-vitro. At 10-25 micrograms ml-1 feverfew had no effect on the formation of arachidonate metabolites while at highest concentrations (50-200 micrograms ml-1) it inhibited both cyclo-oxygenase and lipoxygenase metabolic products.
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Rat isolated intestine incubated in Krebs solution converted exogenous [14C]-arachidonic acid into products that chromatographed with prostaglandins, leukotriene B4 and 5-hydroxy-eicosatetraenoic acid. Accumulation of these products was increased by the laxative ricinoleic acid (0.34 mM) or the calcium ionophore A23187 (7.6 microM). In the presence of the calcium antagonists TMB-8 (0.43 microM) or verapamil (0.2 microM) the mean effects of ricinoleic acid or the calcium ionophore were smaller. Stimulation of arachidonic acid metabolism by ricinoleic acid therefore seems likely to involve a calcium-dependent mechanism.
Inhibition of prostaglandin formation from [14C]arachidonic acid by rat peritoneal leucocytes occurred with nonsteroidal anti-inflammatory drugs, their order of potency being indomethacin greater than piroxicam greater than naproxen greater than ibuprofen greater than isoxicam. At the lowest concentration tested (1 microgram ml-1), indomethacin markedly increased the accumulation of lipoxygenase products in the cell incubates. Naproxen, ibuprofen or piroxicam 1 or 10 micrograms ml-1 resulted in smaller increases of lipoxygenase products, and there was only a small rise with these concentrations of isoxicam.
Rat isolated intestine incubated in Krebs solution converted exogenous [14C]arachidonic acid into products that chromatographed with prostaglandins, leukotriene B4 and 5-hydroxy-eicosatetraenoic acid. The accumulation of these products was increased by phenolphthalein 3.14-1570 microM and reduced by indomethacin 2.8 microM. This raises the possibility that laxation by phenolphthalein involves the formation of arachidonate lipoxygenase and cyclo-oxygenase products.
The antipyretic and antibacterial activities of the ethanolic extract of the flowering tops of Teucrium polium (L.) were been studied. The extract was effective against both yeast and carrageenin pyrexia in rats. It also exhibited a marked antibacterial action against both gram positive and gram negative organisms and was found to be non toxic in acute studies.