الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 207 |  |  |
| | | from | 207 | | |
Abstract
Chronic kidney disease CKD is a global non-communicable health problem. Since fibrosis is considered the base and the fate of CKD, the goal of this study was to set up adenine-induced CKD/fibrosis model and cisplatin-induced CKD/fibrosis model in rats, evaluate the effects of sodium molybdate and paclitaxel on these experimental models and demonstrate the possible involved mechanisms. Both models demonstrated a deterioration in kidney function parameters, revealed severe pathological changes in cortex and medulla in histopathological evaluation of renal tissue sections, and showed a presence of oxidative stress state. In addition, there are an elevation in inflammatory marker, TNF-α level. Furthermore, the induction of fibrosis that determined by Masson’s trichome stain that showed excessive deposition of collagen in cortex and medulla. Additionally, IHC staining of renal sections against TGF-β1 revealed prominent positive glomerular and tubular expression. Moreover, in renal homogenate, Smad3 level was increased and Smad7 level was declined. In conclusion : The results of current study clearly revealed the dose-dependent protective effects of sodium molybdate and paclitaxel on adenine-induced CKD and cisplatin-induced CKD possibly through the suppression of TGF-β/Smad signaling pathway and elevation of Smad7 expression leading to reduction of collagen synthesis, ECM accumulation, and so attenuation of renal fibrosis. Furthermore, they attenuate the inflammation through decreasing the level of TNF-α. Likewise, they reduce the ROS and restore antioxidant molecules, which collectively protect the histological integrity of the kidney. Owing to these results, we suggest that sodium molybdate and paclitaxel may have promising therapeutic value in human in such disorders.