Creation of an adequate animal model of hyperuricemia (acute and chronic hyperuricemia); study of its reversibility and its maintenance.

AIM: Hyperuricemia is defined by the European Rheumatology Society as a uric acid level greater than 6 mg/dl (60 mg/l or 360 µmol/l). Our goal was to evaluate the hypouricemic effect of nettle. For this reason, we have first of all try to create an hyperuricemic animal model which is very suitable because at the level of literature there is not an exact model, there are many models and our objective is to set an adequate model. MATERIALS AND METHODS: An attempt has been made to test acute and chronic hyperuricemia by varying the duration and method of induction of potassium oxonate. Similarly, attempts have been made to induce chronic hyperuricemia through an animal and vegetable diet. The reversibility of hyperuricemia was tested with a maintenance protocol. KEY FINDINGS: For the creation of the hyperuricemia model, it has been shown that acute hyperuricemia cannot be induced by short administration of potassium oxonate and persistent chronic hyperuricemia can be induced only after daily administration of oxonate of potassium by intraperitoneal injection for 15 days. Indeed, hyperuricemia was reversible after stopping the administration of potassium oxonate. The high-purine diet is also capable of inducing chronic hyperuricemia but to a less extent. SIGNIFICANCE: After creating an adequate model of hyperuricemia while setting the dose of potassium oxonate, route of administration and duration. A maintenance protocol was followed which subsequently made it possible to deduce that the daily administration of potassium oxonate must be continued to maintain the hyperuricemia.

Chemoprotective role of ethanol extract of Urtica urens L. against the toxicity of imidacloprid on endocrine disruption and ovarian morphometric in female rats, GC/MS analysis.

Imidacloprid (IMI) is a widely used in Tunisia and abroad, and high doses of IMI have been known to cause endocrine disruption. Some reports claim that Urtica urens L. (UU) can reduce toxicity thanks to it anti-inflammatory and antioxidant activities, but there is no scientific evidence justifying its use, which lets us think to its direct effect on the metabolism of the ovarian tissue. The present study was undertaken to evaluate the protective effect of UU against the toxicity of Confidor®, whose active substance is imidacloprid (IMI), in female rat, as well as the chemical compositions of UU ethanol (EtOH) extract by GC-MS. Female rats were divided into control group, 3 groups treated with IMI at 50, 200 or 300mg/kg/day and three groups co-treated with IMI (50, 200 or 300mg/kg/day)+100mg/kg/day of UU, for 60days. Blood samples were collected for the dosage of 17ß-estradiol levels. Ovaries were removed for tissular dosage of malondialdehyde (MDA), advanced oxidation protein products (AOPP), glutathione (GSH), vitamin E, catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx). Histological and histomorphometric examinations were performed as well. IMI caused an acute ovary injury, increased the ovary tissue levels of MDA and AOPP, and decreased the levels of GSH, vitamin E, and antioxidant enzyme activities. The number and the diameter of follicles were markedly diminished together with a reduction of the relative weight of ovaries. Compared with controls, the treated rats exhibited a significant reduction in serum 17b-estradiol levels. These results suggest an endocrine disruption by IMI which may interfere with ovarian follicles development in rat. The injection of UU EtOH extract improved the histological and all biochemical parameters cited above. In conclusion, IMI induced an acute ovary injury accompanied with disturbance of oxidant status and causes follicular atresia. Significant antioxidant activities were also observed in UU EtOH and a total of 31 compounds were identified. The injection of UU EtOH provided a significant protection which might be due to its antioxidant activities.