Postconditioning with far-infrared irradiation increases heme oxygenase-1 expression and protects against ischemia/reperfusion injury in rat testis

AimsStudies have shown that heme oxygenase-1 (HO-1) has a protective role in the mechanism underlying hypoxic preconditioning. We used a far-infrared radiation (FIR) heater to investigate the postconditioning protective role of HO-1 against ischemia/reperfusion (I/R) injury in rat testis.Main methodsForty rats were used. Testis ischemia was mimicked by total obstructive clamping of testis vessels for 1, 2, or 4 h, and concomitant postconditioning with 30 min FIR or heat light during initially 30 min reperfusion. HO-1 expression and apoptosis of testis tissues were examined by immunohistochemistry and in situ terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) assay, respectively. HO-1 protein level and caspase-3 activity were analyzed by Western blotting.Key findingsThere was less apoptotic activity in rat testis after FIR, as determined by TUNEL assay. Higher HO-1 protein expression was observed by immunohistochemistry and Western blotting (p < 0.01) in testis cells after FIR postconditioning. In contrast, caspase-3 activity was significantly higher in heat light groups, as compared with FIR groups (p < 0.01).SignificanceFIR postconditioning attenuated I/R injury in rat testis by inducing HO-1 expression, which might have a protective role in testis apoptosis after I/R injury.