. The aim of this study was to evaluate the effects of quercetin (QC) and its complex with 2-hydroxypropyl-β-cyclodextrin (QECD) in healing burn related skin wounds in the rat model. Male Wistar rats were subjected to third-degree burn injury of skin in the interscapular area using a metal rod heated to 80 °C. The area of the skin which the burn was applied to was secured from the surroundings by the protective chamber. In order to estimate the efficacy of different treatment modalities the experiments were carried out in two stages. On first stage of the study, the group of animals (n = 21) was subjected to burn injury and the wound surface was not affected with additional procedures except the substances for treatment being applied. During the second stage of the study with another group of animals (n = 18) the removal of necrotic tissue was carried out over the period of 3 to 7 days. The progress of the wound healing was followed by performing morphometric analyses in order to determine complete re-epithelialization. The phagocytic index of neutrophils was determined in washouts from the wounds during the healing process. The animals used on the first stage of the study were sacrificed at day 21 of the experiment and those on the second stage at day 43 and the tissues were subjected to histological examination. The amounts of white blood cells and phagocytic index of neutrophils were calculated in blood samples followed by the measurements of metabolic activities of neutrophils. The removal of necrotic tissue has been found to promote better wound healing caused by thermal exposure. No reliable evidence has been obtained on QC or QECD abilities to significantly accelerate the burn wound epithelialization. The square of the secondary wound scab covered the damaged skin surface has been found to be decreased in the first group of animals on the 14th day followed by the exposure while the rate of wound epithelialization has been found to be increased in the second group of animals at the final stage of wound healing under the treatment with substances being investigated. As a result the ability of QE and QECD to normalize the white blood cell differential, phagocytic and metabolic activities of neutrophils recruited to a wound and neutrophil blood levels has been found.
On the eighth day after ligation of the common bile duct in rats a significant increase in the serum content of total lipids, cholesterol bilirubin and ALT, alkaline phosphatase, and gamma-glutamyltransferase was observed. In the microsomal fraction there was a marked decrease in the content and activity of microsomal monooxygenases. Introperitoneal injection of berberine (10 mg/kg) for 6 days caused a partial normalization of permeability of hepatocytes plasma membranes and activity of microsomal flavin-containing monooxygenases. It is suggested that berberine is a substrate and inducer of flavin-containing monooxygenases. Membrane-stabilizing effect of berberine is probably realized at the level of inhibition of prooxidant status of liver cells.
The hepatoprotective effect of the self-emulsifying composition with berberine was studied in the model of toxic liver damage in rats with acetaminophen and its hepatoprotective properties were analyzed in comparison with the use of berberine in free form. The course introduction of self-emulsifying composition with berberine before intoxication of rats with acetaminophen to a greater extent inhibits the development of cytolysis of hepatocytes, and also promotes the enhancement of the glutathione unit of the antioxidant system, increasing the content of total and free sulfhydryl groups, compared with the introduction of free berberine in animals.
The article is aimed to summarize the scattered data on the role of peroxisome proliferator-activated receptors (PPAR) and the possibility of using PPAR’s agonists for treatment of alcohol dependence and alcoholic liver disease. Earlier it was shown that some PPAR agonists can reduce ethanol consumption and preference in rodents. Several hypotheses considering the antialcoholic activity of PPAR agonists and the roles of PPAR in the development of alcohol dependence were discussed. In light of these data, the therapeutic potential of PPARs agonists as an agent for the treatment of alcoholism, has been reviewed.
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