Research progress for animal hyperuricemia model / 中国药理学通报

ABSTRACT

Hyperuricemia is induced by the mechanism of the elevated production of uric acid or the decreased renal excretion of uric acid. At present, there are three major methods to establish models for hyperuricemia first, it will elicit pronounced hyperuricemia when feeding or injecting the animal with hypoxanthine 600～1000 mg?kg -1 , xanthine 600 mg?kg -1 , adenine 150～300 mg?kg -1 , yeast 15～30 g?kg -1 , uric acid 250 mg?kg -1 or 350～700 mg?kg -1 because of the elevated serum uric acid. Such effect will be also observed as administrating the animal with the inhibitors of uric acid excretion such as ethambutol 250 mg?kg -1 , nicotinic acid 100 mg?kg -1 at the same time of the above steps. Second, being an uricase inhibitor, when fed the rats 0 4 g?d -1 and uric acid 0 6 g?d -1 for 3～4 weeks, oxonic acid is able to cause the continuously elevated serum uric acid. Similarly, when potassium oxonate 300 mg?kg -1 ip only once, the serum uric acid in mice will be also elevated. Third, to destruct the urate oxidase gene (EC 1.7.3.3) in the mouse by homologous recombination in embryonic stem cells, and then the oxidase deficient mutant mouse as the hyperuricemia model, is generated by gene recombination.The rats and the mice have urate oxidase, which can decompose the uric acid to allantoin, while the avian (such as chicken, coturnix and so on) have not.