Drugs online research references
Planta Med. 1995 Dec;61(6):515-8.
Antioxidant activity of fruit exudate and C-methylated dihydrochalcones from Myrica gale.
Mathiesen L, Malterud KE, Sund RB.
Department of Pharmacology, University of Oslo, Norway.
Antioxidant and radical scavenging effects were studied of a diethyl ether extract of the fruit exudate of Myrica gale L., and of C-methylated dihydrochalcones isolated from it. Isolated hepatocytes and liver mitochondria from the rat were incubated with tertbutyl hydroperoxide, and lipid peroxidation measured by the yield of thiobarbituric acid reactive substances. The main antioxidant of the extract, myrigalone B (MyB), inhibited lipid peroxidation in hepatocytes with an IC50 value of 23 +/- 1 microM, whereas in mitochondria the value was 5.2 +/- 0.1 microM. The fruit extract itself inhibited peroxidation in hepatocytes with an IC50 value of 7.0 +/- 0.2 microM calculated according to its MyB content, and in mitochondria with an IC50 of 1.7 +/- 0.1 microM. Other myrigalones were considerably less active or inactive as antioxidants. The IC50 of promethazine, an established inhibitor of lipid peroxidation, was 3.8 +/- 0.4 microM in mitochondria./ Both MyB and the fruit extract caused scavenging of the diphenylpicrylhydrazyl (DPPH) radical with IC50 values of 32 +/- 1 microM and 14 +/- 1 microM (as MyB), respectively. Peroxidation in linoleic acid catalyzed by soybean 15-lipoxygenase was inhibited by MyB (IC50 = 23 +/- 1 microM calculated as MyB; corresponding to an extract concentration of 71 +/- 3 microgram(s)/ml). However, the extract content of myrigalone A, itself a fairly potent inhibitor of 15-lipoxygenase, may contribute significantly to the latter effect.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8824944&dopt=Abstract
Jpn J Pharmacol. 1996 Jun;71(2):109-12.
The role of histamine H1-receptors in the anticonvulsive effect of morphine against maximal electroconvulsive shock in mice.
Karadag CH, Ulugol A, Dokmeci D, Dokmeci I.
Department of Pharmacology, Faculty of Medicine, Trakya University, Edirne, Turkey.
Morphine is known to release histamine from mast cells. It is also known that histamine receptors mediate some of morphine's effects on the central nervous system. The contribution of H1- and H2-receptors to the effect of morphine on maximal electroconvulsive shock in mice was investigated in the present experiments. Morphine showed a dose-dependent anticonvulsive effect, but produced spontaneous clonic convulsions at higher doses (100 mg/kg, i.p.). The anticonvulsive effect of morphine (1 mg/kg, i.p.) was antagonized by histamine H1-receptor antagonists, dimethindene (0.1 mg/kg, i.p.) promethazine (0.4 mg/kg, i.p.) and pheniramine (30 mg/kg, i.p.), and naloxone (10 mg/kg, i.p.), but not by the H2-receptor antagonist ranitidine (10-50 micrograms, i.c.v.). These results show that morphine has an anticonvulsive effect via histamine H1-receptors against maximal electroconvulsive shock in mice.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8835636&dopt=Abstract
Inflamm Res. 1996 Jul;45(7):354-6.
The role of enteric bacteria in the pathogenesis of fatal cycloheximide intolerance in mice pretreated with dexamethasone, promethazine or nordihydroguaiaretic acid.
Parry EW.
Department of Human Anatomy and Cell Biology, University of Liverpool, UK.
As an incidental finding in a separate, ongoing investigation, dexamethasone was shown to sensitise mice fatally to a later challenge with a normally-tolerated dose of cycloheximide. This phenomenon is described here; it is also shown that two unrelated agents, namely promethazine and nordihydroguauaretic acid, duplicated this sensitising effect of the steroid. The three drugs have in common the ability to inhibit powerfully the synthesis of tumour necrosis factor-alpha in response to lipopolysaccharide, and it is suggested that this property is linked to their ability to induce fatal cycloheximide intolerance. Such drug-pretreated mice were protected if given dexamethasone at the time of cycloheximide challenge. An equal degree of protection was conferred on such animals by oral antibiotic treatment known to eliminate the aerobic intestinal flora. This indicated that the three agents induced fatal susceptibility to cycloheximide through the agency of the gut flora. It is proposed that the three drugs act by impairing the hepatic mechanism which normally removes portal vein-borne endogenous lipopolysaccharide, leading to systemic distribution of lipopolysaccharide, which is known from previous work, using a small dose of intraperitoneally injected lipopolysaccharide, to render mice fatally susceptible to a later cycloheximide challenge.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8841837&dopt=Abstract
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