Vitamin E modulates apoptosis and c-jun N-terminal kinase activation in ovarian torsion–detorsion injury

• We investigate the roles of MAPKs in the development of ovarian IR injury.
• The numbers of apoptotic granulosa cells were clearly increased following detorsion.
• Vitamin E ameliorated apoptotic changes in ischemic and reperfused ovarian tissues.
• Enhanced p-JNK activation may be related to increased apoptosis during ovarian IR.
• Vitamin E inhibited p-JNK mediated follicular cell apoptosis in rat ovarian tissue.

The aim of this study was to evaluate the role of vitamin E in follicular degeneration and to assess histopathological and biochemical changes following ischemia–reperfusion (IR) injury in rat ovaries. Twenty-eight Wistar albino rats were randomly divided into four groups: sham, 4 h torsion, 24 h detorsion, and a vitamin E group. Thirty minutes before detorsion, a single dose of 200 mg/kg vitamin E was administered intraperitoneally. The ovarian histology score was determined, serum levels of malondialdehyde (MDA) and myeloperoxidase (MPO) were measured. The apoptosis of granulosa cells and the phospho-c-jun N-terminal kinase (p-JNK) and phospho-p38 (p-p38) immunoreactivities of these cells were determined. MDA and MPO levels were significantly increased in the torsion and detorsion groups. Hemorrhage, edema, and congestion were also apparent in these groups. In addition, the apoptotic index and the immunoreactivity of p-JNK were highest in the detorsion group, which also showed marked follicular degeneration. However, p-p38 activity was not affected by torsion–detorsion (TD) induction. Vitamin E ameliorated TD-induced histological alterations. It also decreased serum levels of MDA and MPO, reduced the activity of p-JNK in the ovaries, and reduced numbers of apoptotic follicular cells. In conclusion, these data indicate that vitamin E attenuated ovarian follicular degeneration by inhibiting the immunoreactivity of p-JNK and reducing the apoptosis of granulosa cells.