Aqueous extract of the leaf and root ofNauclea latifolia Sm. (Rubiaceae) is used in Nigerian folk medicine for the treatment of hypertension. This work is carried out to investigate the effect ofNauclea latifolia leaf extract on lipid profile and cardiovascular activity of rats. Normal and 10% coconut oil fed rats were treated with the water-soluble fraction of the ethanol extract ofNauclea latifolia leaf for 2 weeks. Forty-eight mature male albino rats of the Wistar strain were divided into two experiments of four groups, each group having 6 animals. Experiment I animals were treated with the water-soluble fraction of the ethanol extract whilst experiment II animals were fed 10% coconut oil meal before treatment with the water-soluble fraction of the ethanol extract. A single oral dose ofNauclea latifolia was 170, 340 and 510 mg/kg body wt/day of the extracts respectively for 2 wks. There was no significant change in the lipid profile of the experimental animals as compared with the controls. There was about 40% relaxation on contracted thoracic aorta that was pre-contracted with 2 μM phenylephrine. The viability of the tissue was tested against 10 μM of acetylcholine. There was no significant (P>0.05) change in Na(+) concentration in the serum. However, the K(+) concentration in the serum of the experimental animals showed a significant increase. The study shows that ethanol extract ofNauclea latifolia has vasodilator action on the aorta and that lipid profiles of experimental rats were not affected. Furthermore, the increase in the K(+) may be contributing to the vasodilator effect ofNauclea latifolia.
Proteolytic enzyme activity releasing sialo glycopeptides from 3H-labeled human erythrocyte ghosts was detected in cytotoxic (leukotoxic) culture supernatants from 9 of 12 Pasteurella haemolytica serotypes. Microcrystalline cellulose thin-layer chromatograms of radioactive water-soluble products showed the following two radioactive peaks: a high-mobility minor peak (Rf, 0.54 to 0.74), identified as sialic acid, and a low-mobility major peak (Rf, 0.18 to 0.21), partially characterized as a trichloroacetic acid-soluble, sialic acid-rich fragment with a molecular weight of greater than 3,500, not extractable by chloroform. The sialic acid content of this fragment after treatment with Clostridium perfringens neuraminidase was estimated to be 7.2 X 10(-2) mumol mg-1. The presence of neuraminidase as a separate activity in some culture supernatants was confirmed. It is considered to be responsible for the observed release of free sialic acid. Preliminary studies with the crude enzyme showed that it has a broad pH optimum around pH 7.0 and that activity is not affected by inhibitors of trypsin, chymotrypsin, thermolysin, thio and serine enzymes, nor by an inhibitor of neuraminidase, 2,3-dehydro-2-deoxy-N-acetylneuraminic acid. Activity was, however, inhibited by o-phenanthroline at a high concentration after prolonged treatment. The enzyme hydrolyzed glycophorin at a rate four times higher than the rate for casein. Free glycophorin inhibited the enzyme-induced release of radioactive products from 3H-labeled ghosts. It is speculated that the novel enzyme is a neutral protease, probably metal-dependent, with specificity for sialoglycopeptides. The possible relationship of this protease to the previously reported host species-specific leukotoxicity of P. haemolytica and its potential role in virulence is discussed.
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