Protective effect of ligustrazine on oxidative stress and apoptosis following testicular torsion in rats

Testicular torsion is a common urologic emergency and one of the causes of infertility in males. It has been reported that ligustrazine may decrease oxidative stress and reduce ischemia–reperfusion injury. This study aims to investigate the protective effect of ligustrazine in ischemia–reperfusion injury after testicular torsion-detorsion. First, 40 rats were randomly and equally divided into TMP (Ligustrazine) group, the Testicular torsion (T/D) group, the Sham (Sham operation) group, and Control group. The left testis of rats in the TMP and T/D group was rotated for 2 h. The TMP group was intraperitoneally injected with ligustrazine solution and the T/D and the Sham groups were injected with normal saline. The left testes of four groups were obtained for assay on the 4th day after the operation. Average level of superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT) were higher in Sham and Control groups than T/D group and TMP group. Conversely, average level of malondialdehyde (MDA) and reactive oxygen species (ROS) was lower in Sham and Control groups than T/D group and TMP group. In contrast with the T/D group, SOD, GPX, and CAT enzymatic activities increased, whereas MDA and ROS content decreased in the TMP group (P < 0.05). Microscopic observation showed that the testicular tissue of the Sham and Control groups were basically normal. The TMP and T/D groups had significant testicular tissue damage, whereas the TMP group had less damage and apoptosis than the T/D group. The apoptotic index of germ cells in the TMP group (13.05 ± 4.41) was lower than the T/D group (30.23 ± 11.31) (P < 0.05) and higher (P < 0.05) than the Sham group (0.56 ± 0.29). So we found that Ligustrazine lowered ischemia–reperfusion injury after testicular torsion-detorsion by decreasing the reactive oxygen species and suppressing apoptosis.