Abstract
Hyperuricemia has been considered to be a key risk factor for kidney disease. The
formation of uric acid crystals in the kidney further stimulates an intensive inflammatory
response. Rhein possesses various pharmacological activities, including anti-inflammatory,
antioxidative, antitumor, purgative effects, and so on. To our knowledge, no previous
work has been reported about the therapeutic effect of rhein on urate nephropathy.
In this study, a model of hyperuricemia and nephropathy induced by adenine and ethambutol
in mice was established. Meanwhile, the potential beneficial effects and mechanisms
of rhein on hyperuricemia and nephropathy were also investigated. The results demonstrated
that rhein significantly decreased the serum uric acid level by inhibiting the xanthine
oxidase activity and increasing the excretion of urinary uric acid. In addition, rhein
also markedly improved kidney damage related to hyperuricemia. Further investigation
indicated that rhein improved the symptoms of nephropathy through decreasing the production
of proinflammatory cytokines, including interleukin 1β, prostaglandin E2, and tumor necrosis factor-α and inhibiting the expression of transforming growth factor-β1. The present study suggests that rhein may have a considerable potential for development
as an anti-hyperuricemic and nephroprotective agent for clinical application.
Key words
rhein - hyperuricemia - nephroprotective effect - xanthine oxidase - uricosuric action
- interleukin-1
β
- transforming growth factor-
β1