Evaluation of inflammatory and fibrogenetic responses in rat kidneys following unilateral partial ureteral obstruction

Aim: Although various animal models of complete or partial unilateral ureteral obstruction (UUO) have been used to elucidate the etiopathogenesis of renal injury, the specific roles of inflammatory and fibrogenetic pathways remain inadequately understood. This study aimed to investigate the involvement of IL-6 and STAT3 in inflammation and fibrogenesis in a rat model of partial UUO using immunohistochemical techniques. Materials and Methods: Eighteen 21-day-old Wistar rats were randomly assigned into three groups (n=6 per group): control (C), sham (S), and partial ureteral obstruction (PUO). No surgical procedure was performed in the control group. In the sham group, the left proximal ureter was dissected free from the psoas muscle after laparotomy without obstruction. In the PUO group, the left proximal ureter was similarly dissected but then embedded into the psoas muscle at two points to induce partial obstruction. After a 14-day experimental period, all animals were sacrificed. Ipsilateral nephrectomy specimens were collected and analyzed for IL-6 and STAT3 expression using immunohistochemical methods. Results: In the early postoperative period (first two weeks), IL-6 expression was significantly higher in the S and PUO groups compared to the control group (p<0.0001). Although IL-6 levels were higher in the PUO group than in the S group, this difference was not statistically significant (p>0.05). Similarly, STAT3 expression was elevated in the PUO group compared to both the C and S groups, yet the difference did not reach statistical significance (p>0.05). Conclusion: The significant increase in IL-6 expression in the PUO group compared to controls, along with its elevated—albeit non-significant—levels compared to the sham group, suggests a potential role for IL-6 in early inflammatory and fibrogenetic responses. The non-significant increase in STAT3 expression may indicate an early-stage activation of fibrogenetic signaling. Further long-term studies incorporating additional molecular pathways are warranted to better understand the mechanisms underlying PUO-induced renal injury.