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Regardless of these effects the exact molecular mechanisms of Quercetin remain uncertain. Nam and colleagues by way of example showed that Quercetin at a concentration as minimal as 20��M induced apoptotic cell death from the mouse osteoblastic cell line MC3T3-E1 in an ERK1/2-dependent method [17]. These information are at variance with earlier reviews in which Quercetin will not induce cell death in rat calvaria osteoblastic cells [18], MC3T3-E1 cells [19], and MG-63 human osteoblastic cells [20]. In our model Quercetin induced phosphorylation of ERK1/2; having said that, lowered cell viability was only observed soon after 24h exposure at concentrations above 200��M. Highlighting the discrepancy towards the findings of Nam and colleagues we obtained substantial protective effects of Quercetin at concentrations comparable to physiological relevant plasma amounts. Furthermore, the capability to cut down ROS was not observed at concentrations under 50��M in osteoclasts as described by Wattel and coworkers [10]. Nevertheless, even concentrations as reduced as 25��M of Quercetin safeguard primary human hepatocytes from ethanol-induced injury [11, 12].However, in spite of our observed constructive effects, it's necessary to remain cautious when analyzing its clinical possible.

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