چاپ صفحه |  صفحه نخست سامانه |  چکیده مقاله |  نویسندگان |  دانلود مقاله | دانشگاه علوم پزشکی تبریز |
| Renal fbrosis is characterized by accumulation of extracellular matrix components and collagen deposition. TGF-β1 acts as a master switch promoting renal fbrosis through Smad dependent and/or Smad independent pathways. Thirty-fve male C57BL/6 mice were divided into fve groups of seven each; sham, unilateral ureteral obstruction (UUO), UUO+galunisertib (150 and 300 mg/kg/day), galunisertib (300 mg/kg/day). The UUO markedly induced renal fbrosis and injury as indicated by renal functional loss, increased levels of collagen Iα1, fbronectin and α-SMA; it also activated both the Smad 2/3 and MAPKs pathways as indicated by increased levels of TGF-β1, p-Smad 2, p-Smad 3, p-p38, p-JNK and p-ERK. These UUOinduced changes were markedly attenuated by oral administration of galunisertib, the TGFβRI small molecule inhibitor. In conclusion, we demonstrated that TGF-β1 receptor blockade can prevent UUO-induced renal fbrosis through indirect modulation of Smad and MAPKs signaling pathways and may be useful as a therapeutic agent in treatment and/or prevention of renal fbrosis. |
| نویسنده | نفر چندم مقاله |
|---|---|
| سعید نظری سلطان احمد | اول |
| مهران مسگری عباسی | نهم |
| نام فایل | تاریخ درج فایل | اندازه فایل | دانلود |
|---|---|---|---|
| 2022TGFB1 receptor blockade attenuates UUOinduced renal fibrosis.pdf | 1401/04/05 | 2973887 | دانلود |
