Background
Ureteral thermal injury (UTI) occurs when the ureter is exposed to high temperatures during surgical procedures, leading to tissue damage and ureteral stricture. Dexamethasone (DEX) has been widely used to treat a variety of diseases for its anti-inflammatory and immunosuppressant effects. However, its role in treating UTI remains unclear. The
Conclusions
DEX reduces the severity of renal fibrosis and inflammation after UTI and exerts a significant renal protective effect.
Methods
Thirty C57BL/6J mice were randomly divided into three groups (n=10 per group): (I) control group, (II) UTI group, (III) UTI + DEX group. UTI mouse models were constructed using a fast-pack pro-obturation pack handpiece instrument, and the therapeutic effect of DEX (2.5 mg/kg) on UTI was investigated via intraperitoneal injection for two weeks. Pathological changes in the ureter, renal function, extracellular matrix protein deposition, and inflammatory markers in the kidneys were evaluated in mouse models.
Results
Ureteral histopathological changes were more severe in the UTI group than in the control group; however, DEX treatment alleviated these changes to a certain extent. Mice in the UTI group exhibited elevated renal function. Although DEX alleviated renal function deterioration, the difference was not statistically significant. Moreover, in comparison to the control group, kidney samples from the mice in the UTI group revealed increased messenger RNA (mRNA) levels of inflammation markers, indicating a progressive inflammation response, while DEX significantly reversed interleukin-1β (IL-1β) expression at the protein level. Additionally, fibrosis-related markers were markedly increased in the kidneys of UTI mice. These findings were significantly reversed by DEX treatment, revealing its anti-inflammatory and anti-fibrotic activities. Conclusions: DEX reduces the severity of renal fibrosis and inflammation after UTI and exerts a significant renal protective effect.