Drugs online research references
Antimicrob Agents Chemother. 1993 Nov;37(11):2459-65.
Experimental visceral leishmaniasis: role of trans-aconitic acid in combined chemotherapy.
Kar S, Kar K, Bhattacharya PK, Ghosh DK.
Leishmania Group, Indian Institute of Chemical Biology, Calcutta.
We previously reported the effectiveness of trans-aconitic acid (TAA) as an antileishmanial compound. Inhibitory effects of TAA along with other antileishmanial compounds on transformation and in vitro multiplication in macrophage cultures of Leishmania donovani have been assessed. The efficacy of TAA in combined chemotherapy of experimental visceral leishmaniasis has also been evaluated along with those of commonly used antileishmanial compounds such as sodium stibogluconate, pentamidine, and allopurinol. TAA (2 mM) inhibited transformation of L. donovani amastigotes to promastigotes by 95.2%, whereas in combination with pentamidine (5 micrograms/ml), allopurinol (10 micrograms/ml), and sodium stibogluconate (50 micrograms of Sb per ml), it inhibited transformation by about 100, 99, and 98.5%, respectively. Sodium stibogluconate (20 micrograms of Sb per ml), pentamidine (2 micrograms/ml), and allopurinol (5 micrograms/ml) suppressed the amastigote burden in peritoneal macrophage cultures from BALB/c mice by 32.6, 56.1, and 46.3%, respectively. When these three drugs were used along with TAA (5 mM), the parasite loads were reduced by 100, 100, and 88.1%, respectively. TAA (5 mM) alone suppressed the amastigote burden by 59.5%. In experimental visceral leishmaniasis in hamsters (1-month model), TAA at a dose of 200 mg/kg of body weight per day suppressed the spleen parasite load by 73.5%, and TAA in combination with sodium stibogluconate (50 mg of Sb per kg per day), pentamidine (8 mg/kg/day), and allopurinol (15 mg/kg/day) inhibited the spleen parasite load by 98, 98.9, and 97%, respectively. Individually, these three drugs inhibited the parasite load by 35, 20, and 22%, respectively. TAA (400 mg/kg/day) inhibited the spleen parasite load by 99.8%, but an inhibitory effect of approximately 100% was noted when TAA was supplemented with an antileishmanial drug. TAA was administered in experimental animals through oral, intraperitoneal, and intramuscular routes; the intramuscular route was most effective.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8285634&dopt=Abstract
J Pharm Pharmacol. 1993 Jun;45(6):535-9.
Role of polymorphonuclear leucocytes and oxygen-derived free radicals in the formation of gastric lesions induced by HCl/ethanol, and a possible mechanism of protection by anti-ulcer polysaccharide.
Matsumoto T, Moriguchi R, Yamada H.
Oriental Medicine Research Center, Kitasato Institute, Tokyo, Japan.
This study examined the role of oxygen-derived free radicals in the pathogenesis of gastric mucosal lesions induced by HCl/ethanol. Superoxide dismutase, and catalase, and their combination reduced gastric lesion formation in mice. Gastric lesions were also reduced in mice treated with cyclophosphamide or anti-neutrophils, but not in mice treated with allopurinol or desulphated-carrageenan. Cobra venom factor did not reduce lesion formation. These results suggested that oxygen-free radicals may contribute to the formation of gastric mucosal lesions induced by HCl/ethanol, and that oxygen radicals were generated from neutrophils but not from xanthine oxidase. Anti-ulcer pectic polysaccharide, bupleuran 2IIc, which was recently isolated from the roots of Bupleurum falcatum L., showed potent inhibition of HCl/ethanol-induced gastric lesions in mice. Bupleuran 2IIc seemed to scavenge hydroxyl radical effectively. It was suggested that this anti-ulcer polysaccharide may provide protection to the gastric mucosa by scavenging oxygen-free radicals.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8103101&dopt=Abstract
Gen Pharmacol. 1996 Apr;27(3):545-50.
Role of polymorphonuclear leukocytes and oxygen-derived free radicals in chronic gastric lesion induced by acetic acid in rat.
Motilva V, Martin MJ, Luque MI, Alarcon de la Lastra C.
Laboratorio de Farmacologia y Farmacodinamia, Facultad de Farmacia, Universidad de Sevilla, Spain.
This study examined the role of oxygen-derived free radicals, the potential involvement of neutrophils and the possible mucosal vascular permeability changes involved in the pathogenesis and evolution of gastric mucosal lesions induced by acetic acid in the rat. Myeloperoxidase activity was assayed and used as an index of leukocyte infiltration. Application of acetic acid produced a significant increase in this activity 7 and 14 days after induction of chronic injury. Administration of hydroxyurea intraperitoneally was associated with a decrease in the severity of chronic ulceration and neutrophil infiltration into the gastric lesion. This effect was detectable enzymatically and microscopically. Orally administered allopurinol did not produce any beneficial effects on either the macroscopic and histological appearance or on vascular permeability. These results suggest that oxygen-derived free radicals may contribute to the formation and development of chronic lesions and that oxygen-derived free radicals were generated from neutrophils, but not from the xanthine oxidase pathway. These inflammatory cells may, therefore, have a lesive role in the origin and course of acetic acid ulcer disease.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8723542&dopt=Abstract
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