Treatment with pravastatin attenuates oxidative stress and protects osteoblast cell viability from indoxyl sulfate.

Chronic kidney disease has a high level of oxidative stress, a phenomenon that is induced, at least in part, by the accumulation of uremic toxins. Several reports have revealed that indoxyl sulfate, one of the uremic toxins, accelerates oxidative stress in chronic kidney disease. On the other hand, it is also well known that statins have pleiotropic effects; however, it still remains unclear whether statins suppress osteoblastic cell dysfunction or cytotoxicity induced by uremic toxins. To elucidate whether statins ameliorate osteoblast dysfunction induced by uremic toxins, we conducted an in vitro study using primary cultured osteoblastic cells from mouse calvariae. Indoxyl sulfate induced reactive oxygen species production and reduced cell viability in osteoblastic cells in a dose dependent manner. The addition of pravastatin suppressed reactive oxygen species production and ameliorated cell viability. These data suggest that pravastatin attenuates oxidative stress and protects osteoblastic cell viability from indoxyl sulfate.