Carvacrol containing products such as Origanum onites have been used as phytotherapeutic agents in the treatment of serious skin injury. It has been suggested that carvacrol is the active component of these herbs because of its anti-microbial property. With the anti-microbial activity and as an ingredient of these herbs, carvacrol is a promising molecule for the treatment of skin injury. In the present study, we have evaluated the efficacy of carvacrol on healing progress after excisional skin injury. Here, Wistar-Albino rats were divided into two groups and treated with carvacrol and vehicle. Carvacrol was administrated topically at a concentration of %12.5 for the 5 consecutive days after excisional skin injury. Tissue samples were harvested on days 3 rd , 8th and 12 th after injury. Significant beneficial effect of carvacrol was observed at the end of the experiment. In the acute phase of the injury, carvacrol treatment increased tissue granulation and decreased wound depth moderately. These effect of carvacrol was associated with increased TNF-α. However, at the second half of the experiment the elevated level of TGF-B 1 was observed as compared with control animals. The level of IL-1 β was increased in carvacrol treated animals only on day 8. Here, we provide evidence that carvacrol improves wound healing by regulating pro-inflammatory molecules TNF-α, IL-1 β and TGF-β 1 .

The present study was designed to investigate and compare the effects of dietary selenium (Se) and vitamin E on some physiological parameters and histological changes in liver, heart, and skin tissues, as well as the blood parameters and the related enzymes. Both sex young rabbits were fed with deficient (9.8 micrograms/kg diet), adequate (225 micrograms/kg diet), and rich (4.2 mg/kg diet) Se and vitamin E diets for 12-15 wk for this purpose. As the plasma Se levels and the erythrocyte glutathione (GSH) peroxidase activity decreased (79.8 +/- 9.4 ng/mL and 2.0 +/- 0.3 U/g Hb, respectively) in the deficient group, these values increased (100.4 +/- 2.7 ng/mL and 14.5 +/- 4.3 U/g Hb) in the rich group significantly with respect to the control group. The other antioxidant enzyme activities and the related element levels did not change significantly in either one of the experimental groups. Although the platelet counts of the two experimental groups were not different from the control values, the collagen and the adenosine diphosphate (ADP) stimulated platelet aggregation rate and intensity increased in the deficient group (p < 0.05) and decreased very significantly (p < 0.001) in the rich group. In both of the experimental groups, as the percentage values of the neutrophils decreased, the lymphocytes and the eosinophils increased significantly. According to the light microscopic investigations, the observed lesions of considerable intensity within the tissues that elicit cell degenerations were more pronounced in the animals fed with the rich diet than in those fed with the deficient diet. The deficiency as well as toxicity of Se and the deficiency of vitamin E caused several alterations in the physiological functions of the tissues, and these alterations were supported by the histological lesions within these tissues.

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The platelet-activating factor (PAF) is an inflammatory mediator and it may exert some of its effects by reactive oxygen species (ROS). We investigated the effects of PAF and hyperbaric oxygenation (HBO) on copper (Cu) and zinc (Zn) levels in plasma and the intracellular antioxidant enzyme activities of rats. PAF administration caused a decrease in erythrocyte catalase (CAT) and glutathione peroxidase (GPx) activities and in the plasma zinc level. Following PAF administration, exposure to HBO also caused a decrease in erythrocyte GPx activity. These results support the hypothesis that PAF may produce free oxygen radicals and HBO enhances this effect. The enzyme activities of the antioxidant defense system were found to be affected by these oxidative processes. This is likely to be the result of excessive production of ROS or overutilization and/or inhibition of the antioxidant enzymes.

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