Ononenyi, Chimezie U.2009-06-012009-06-012009-04-08http://purl.umn.edu/50551Additional contributors: Joynal Abedin; Shunan Li; Betsy Kren; Mark Rosenberg; Cliff Steer; Sandeep Gupta (faculty mentor).Presently there is no therapy for acute kidney injury (AKI). Potentially one can protect kidneys against injury by preventing cell death following AKI. There are two types of cell death that occurs following AKI: necrosis and apoptosis. Necrosis is uncontrolled and synchronous cell death that occurs at the time of AKI. In contrast, apoptosis, or programmed cell death is an asynchronous cell death that continues to occur for days following AKI, thereby providing a window of opportunity for intervention. Tauroursodeoxycholic acid (TUDCA), a bile acid synthesized in the liver, has been shown to be effective by inhibiting apoptosis in rat models of stroke and Huntington’s disease. We hypothesized that TUDCA will be similarly effective in protection against AKI. Accordingly, the goal of this study was to investigate the protective effects of TUDCA in a rat model of ischemic AKI. We induced AKI by bilateral renal artery clamping for 45 minutes. Three rats were given 400mg/kg/day of TUDCA intraperitoneally from day -1 to day 6, while the control animals received the vehicle. We determined kidney functions by measuring blood urea nitrogen (BUN), proliferation by immunohistochemistry for Ki67, and apoptosis by TUNEL assay. Compared to a control, animals that received TUDCA had less severe kidney injury and apoptosis. In conclusion, TUDCA provides protection against acute kidney injury likely by preventing apoptosis.en-USCollege of Biological SciencesBiology ProgramAcademic Health CenterDepartment of MedicineStem Cell InstitutePresentation