Protective effect of Urtica dioica in induced neurobehavioral changes, nephrotoxicity and hepatotoxicity after chronic exposure to potassium bromate in rats.

BACKGROUND AND PURPOSE: Chronic exposure to potassium bromate (KBrO3), a toxic halogen in the environment, has become a global problem of public health. The current study aims to elucidate for the first time the effect of Urtica dioica (UD) on behavioural changes, oxidative stress, and histopathological changes induced by KBrO3 in the cerebellum, kidney, liver and other organs of adult rats. STUDY DESIGN AND METHODS: The rats were divided into four groups: group 1 served as a control received physiological serum, Group 2 received KBrO3 (2 g/L of drinking water), group 3 received KBrO3 and Urtica dioica (100 mg/kg), and group 4 received KBrO3 and Urtica dioica (400 mg/kg). We then measured behavioural changes, oxidative stress, and biochemical and histological changes in the cerebellum, liver, kidney and others organs in these rats. After 30 days of treatment, the animals were sacrificed. RESULTS: We observed significant behavioural changes in KBrO3-exposed rats. When investigating redox homeostasis in the cerebellum, we found that mice treated with KBrO3 had increased lipid peroxidation and protein oxidation in the cerebellum. In addition, it inhibits hepatic and lipid peroxidation (malondialdehyde), advanced oxidation protein product (AOPP), attenuates KBrO3-mediated enzyme depletion, catalase, superoxide dismutase, glutathione peroxidase enzymatic and antioxidant activities in the liver and kidney. Rats that were co-managed with Urtica dioica at the high portion of 400 mg/kg indicated a higher effect than that treated with the low dose of 100 mg/kg practically in all the tests carried out. CONCLUSION: Our results demonstrate that Urtica dioica is a potential therapeutic agent for oxidative stress associated with neurodegenerative diseases.

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.