Additionally, ICP-MS data revealed that fisetin did not alter the renal uptake of cisplatin. Hence, we suggest, fisetin by virtue of its free radical scavenging properties attenuates the cisplatin-induced nephrotoxicity in rats. In conclusion, the results of the present study clearly demonstrated the renoprotective effect of fisetin against cisplatin-induced acute renal injury in rats. The mechanisms underlying the renoprotective effect of fisetin could be by reducing oxidative stress, restoring mitochondrial respiratory Caffeic Acid Phenethyl Ester enzyme activities and suppressing apoptosis in renal tissues. In addition, the BRL-54443 mechanism of this renoprotective effect may also involve inhibition of NF-kB activation and attenuation of subsequent pro-inflammatory mediators release in kidney tissues. However, further studies are needed to explore the additional mechanisms responsible for renoprotective effect of fisetin and to establish its feasible use in clinical setup as an adjunct candidate to cisplatin therapy. Cholesteatoma is a tumorous growth of keratinizing squamous epithelia in the middle ear that is reported to affect around 7�C9 people per 100.000/year in Europe. The observed expansive, destructive, and invasive characteristics share similarities with malignant diseases, which is mirrored by the extensive surgery and control regimens. Most patients experience severe complications ranging from hearing loss to potentially fatal intracranial infections, and there is a pressing need for developing medical treatment alternatives, based on the molecular pathology. The basis for the development of cholesteatoma is ectopic keratinizing epithelial cells in the middle ear cavity, but its etiopathogenesis is not fully understood. The introduction of keratinizing epithelia to the middle ear is thought to arise mainly from retraction-pockets and/or thinning of the tympanic membrane, which are prevalent conditions in middle ear pathology, but may also stem from the immigration of cells through tympanic membrane perforations, metaplasia of the middle ear keratinocytes, migration of external auditory canal keratinocytes, and embryonic remnants.