betadex has been researched along with Poisoning* in 4 studies
4 other study(ies) available for betadex and Poisoning
Article | Year |
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Comparative analysis of protective effects of curcumin, curcumin-β-cyclodextrin nanoparticle and nanoliposomal curcumin on unsymmetrical dimethyl hydrazine poisoning in mice.
The aim of this study was to compare the protective effects of curcumin, curcumin-β-cyclodextrin nanoparticle curcumin (BCD-CUR) and nanoliposomal curcumin (NLC) on unsymmetrical dimethylhydrazine (UDMH) induced poison in mice. Curcumin, BCD-CUR, and NLC were prepared and their properties of zeta potential, particle size, encapsulation efficiency, and loading capacity were characterized. Eighty-eight male ICR mice on normal chow diet were randomly divided into 11 groups, and intraperitoneally injected with UDMH alone, or together with different doses of curcumin, BCD-CUR or NLC daily for up to 10 d. Enzyme activities of serum alanine transaminase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) were analyzed by fully-automatic analyzer and neurotransmitter levels were determined with high performance liquid chromatography (HPLC). 150 mg/kg curcumin treatment alone significantly reduced levels of serum ALT and LDH that were induced by UDMH and markedly increased level of γ-amino butyric acid (GABA) that were reduced by UDMH in the hippocampus. 150 mg/kg BCD-CUR not only decreased significantly the increase of ALT, LDH and glutamate (Glu) but also recovered levels of AST and GABA. 150 mg/kg NLC recovered profoundly levels of AST and GABA while decreased remarkably the UDMH induced increase of ALT, LDH, Glu and 5-hydroxytryptamine (5-HT). In addition, treatments with all tested doses of NLC significantly reduced the UMDH induced dopamine (DA), the monoamine neurotransmitter. NLC had more profound protective effects against liver and central nervous system injury induced by UDMH than a suspension of BCD-CUR or curcumin did in mice. Topics: Alanine Transaminase; Animals; Aspartate Aminotransferases; beta-Cyclodextrins; Central Nervous System Diseases; Curcumin; Dimethylhydrazines; Dose-Response Relationship, Drug; gamma-Aminobutyric Acid; Hippocampus; L-Lactate Dehydrogenase; Liver; Male; Mice; Mice, Inbred ICR; Nanoparticles; Particle Size; Poisoning | 2016 |
Cyclodextrines as functional agents for decontamination of the skin contaminated by nerve agents.
Three decontamination solutions of beta-cyclodextrines were prepared. Their abilities to decontamine rat skin contamined with nerve agent soman were tested. Decontamination efficacy of the tested cyclodextrine solutions was compared with the same decontamination means but without the cyclodextrines. The efficacy of tested decontaminants was evaluated by the assessment of the ID50 values. Two decontamination prescriptions with cyclodextrines (tetraborate buffer and tetraborate buffer with acetone) do not show significantly better decontamination efficacies in comparison with prescriptions without cyclodextrines. Only in case of aqueous solution of 2-aminoethanol the addition of beta-cyclodextrine resulted in significant increase (32%) in decontamination efficacy. Topics: Animals; beta-Cyclodextrins; Chemical Warfare Agents; Cholinesterase Inhibitors; Cyclodextrins; Decontamination; Male; Poisoning; Rats; Rats, Wistar; Skin Absorption; Soman | 2004 |
Evaluation of hydroxypropyl-beta-cyclodextrin in the treatment of aldicarb poisoning in rats.
Cyclodextrins are ring-shaped oligosaccharides with a hydrophilic exterior and a hydrophobic interior. The interior cavity is capable of complexing fat-soluble molecules small enough to fit inside. Sprague-Dawley rats were used to evaluate the efficacy of hydroxypropyl-beta-cyclodextrin as treatment of aldicarb poisoning in rats. Survival times in the majority of rats dosed with aldicarb and receiving intravenous cyclodextrin were longer compared with the control rats only dosed with aldicarb per os. Topics: 2-Hydroxypropyl-beta-cyclodextrin; Administration, Oral; Aldicarb; Animals; beta-Cyclodextrins; Dose-Response Relationship, Drug; Excipients; Injections, Intravenous; Insecticides; Male; Poisoning; Random Allocation; Rats; Rats, Sprague-Dawley; Treatment Outcome | 2004 |
Development of a toxin-binding agent as a treatment for tunicaminyluracil toxicity: protection against tunicamycin poisoning of sheep.
To assess the ability of certain derivatives of beta-cyclodextrin to treat sheep affected by tunicaminyluracil toxicity, using tunicamycin poisoning as a model system.. Controlled treatment trial.. One hundred and sixty Merino wethers were used in the studies.. Groups of sheep were experimentally poisoned with tunicamycin. Derivatives of beta-cyclodextrin, with or without magnesium sulphate and magnesium gluconate, were administered to treatment groups daily for 2 to 3 days. Treatment groups were compared with untreated groups in terms of survival.. A significant increase in survival was observed following treatment of tunicamycin-affected sheep with hydroxypropyl-beta-cyclodextrin (HP beta-CD) and magnesium sulphate in solution (P < 0.05). In subsequent trials, formulation of the cyclodextrin in the form of a magnesium gluconate gel suspension demonstrated significant protection (P < 0.01) and was equally as effective as the cyclodextrin in solution, but required half the frequency of administration, even when the treatment was not commenced until 24 h after the final toxin dose. Beta-cyclodextrin-epichlorohydrin copolymer also improved the survival rate. After toxin administration, the sheep lost significantly less weight if treatment with HP beta-CD was commenced early (P < 0.001).. Protection studies using these two beta-cyclodextrin derivatives suggest that they may be effective in increasing the survival of sheep poisoned by tunicamycin and warrant further testing in field outbreaks of annual ryegrass toxicity. Topics: Animals; beta-Cyclodextrins; Body Weight; Cyclodextrins; Disease Models, Animal; Male; Poisoning; Sheep; Sheep Diseases; Tunicamycin | 1998 |