Abstract
Background. Renal ischemia-reperfusion injury (IRI) is one of the inevitable complications of surgery. The evidence shows that fingolimod, with its anti-inflammatory effects, can play a protective role in renal IRI. The main aim of the present study was to investigate the role of fingolimod against renal IRI in the heart tissue.
Methods. Twenty-four male Wistar rats (220±20g) were treated with a single dose of fingolimod (1mg/kg) by intraperitoneal injection before the induction of kidney IRI. At the end of the reperfusion period, the oxidative stress biomarker (malondialdehyde) and antioxidant biomarkers (catalase, superoxide dismutase, glutathione, glutathione peroxidase, and total antioxidant capacity) were evaluated in the heart tissue.
Results. Fingolimod pretreatment could increase cardiac glutathione enzyme activity in the fingolimod+IR group compared to the IR group, which was not statistically significant (P>0.05). The level of total antioxidant capacity in the heart tissue was also significantly increased in the fingolimod+IR group in comparison to the IR group (P<0.05).
Conclusion. Fingolimod was able to prevent oxidative stress damage in the heart caused by kidney IR induction by increasing the level of total antioxidant capacity of the heart tissue. It is suggested that future studies evaluate the effects of this drug in clinical trials.
Practical Implications. The total antioxidant capacity of the heart, as a distant organ affected by kidney IRI, is increased following fingolimod pre-treatment.