The aim of the present study was to examine the protective effects of the
urinary trypsin inhibitor ulinastatin (UTI) on renal interstitial
inflammation and
fibrosis in rats subjected to unilateral
ureteral obstruction (UUO). A total of 24 male Wistar rats were randomly divided into the three groups; the
sham operation (SOR) group (n=8), the UUO group (n=8) and the UUO+UTI group (post‑UUO UTI treatment, n=8). UUO was performed with complete
ligation of the left ureter. As a medical intervention, saline (4 ml kg‑1 d‑1) and UTI (40000 units kg‑1 d‑1) were injected, respectively, into the animals of the corresponding groups on day one following surgery. The rats in all three groups were euthanized on day seven post surgery. Blood samples were harvested for blood
urea nitrogen (BUN) and serum
creatinine (Scr) content measurements. The degree of interstitial pathological changes in the tissues from the obstructed kidneys were observed through
hematoxylin and
eosin (H&E) and Masson staining. The CD68+ macrophage amount,
tumor necrosis factor‑α (TNF‑α),
interleukin 1β (IL‑1β), nuclear factor‑κB (NF‑κB), transforming growth factor‑β1 (TGF‑β1) and
type I collagen (Col‑I) levels were examined immunohistochemically. The
protein expression levels of NF‑κB were examined using western blot analysis. Total
superoxide dismutase (SOD) activity and
malondialdehyde (MDA) content of homogenates were measured spectrophotometrically. The results revealed that
ulinastatin had no statistically significant effect on the BUN and Scr levels (P>0.05). However, in comparison with the SOR group, the UUO group exhibited significantly more severe renal interstitial pathological injury in terms of tubular dilation, epithelial
atrophy, renal interstitial inflammatory cell infiltration and proliferation of fibrous tissues, as well as significantly elevated levels of interstitial CD68+ macrophages, IL‑1β, TNF‑α, NF‑κB, TGF‑β1 and Col‑I (P<0.01). UTI treatment significantly reduced UUO‑induced renal interstitial damage with reduced levels of interstitial CD68+ macrophages, IL‑1β, TNF‑α, NF‑κB, TGF‑β1 and Col‑I and MDA (P<0.05), and increased SOD levels (P<0.05). In conclusion, the present study indicated that UTI is able to effectively inhibit UUO‑side renal interstitial inflammatory reaction and
fibrosis in UUO‑inflicted rats.