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Fig. 5 | Arthritis Research & Therapy

Fig. 5

From: Lesinurad, a novel, oral compound for gout, acts to decrease serum uric acid through inhibition of urate transporters in the kidney

Fig. 5

Lesinurad is not toxic to mitochondria (a) and does not induce peroxisome proliferator-activated receptor gamma (PPARγ) (b). Different doses of lesinurad (closed squares), benzbromarone (open triangles), or probenecid (open squares) were incubated with cells. a Mitochondrial membrane potential was measured in HepG2 cells. Lesinurad and probenecid did not change the membrane potential at any of the doses tested, whereas benzbromarone at the same concentrations altered the membrane potential in a dose-dependent manner, indicative of mitochondrial toxicity. Each point was performed in triplicate and is presented as mean ± SEM. b PPARγ activation was measured in cells expressing a PPARγ-responsive reporter gene. Lesinurad has no effect, although probenecid mildly induces PPARγ at the highest concentration tested. Benzbromarone strongly induces PPARγ activity. The effects of benzbromarone on perturbing hepatic mitochondrial function and activating PPARγ may lead to hepatotoxicity and cardiovascular events, respectively

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