Research reportNeuroprotective effects of silymarin on ischemia-induced delayed neuronal cell death in rat hippocampus

- The delayed neuronal cell death occurred in the hippocampus of ischemic rats.
- The delayed neuronal cell death was likely to be due to autophagy.
- Silymarin showed neuroprotective effects on this delayed neuronal cell death.
- The neuroprotective effects of silymarin did not depend on the timing of application.

We examined the effects of silymarin, which was extracted from Silybum marianum, on delayed neuronal cell death in the rat hippocampus. Rats were divided into four groups: sham-operated rats (sham group), rats which underwent ischemic surgery (control group), rats which were treated with silymarin before and after ischemic surgery (pre group), and rats which were treated with silymarin after ischemic surgery only (post group). We performed the ischemic surgery by occluding the bilateral carotid arteries for 20 min and sacrificed the rats one week after the surgery. Silymarin was administered orally at 200 mg/kg body weight. Smaller numbers of delayed cell deaths were noted in the rat CA1 region of the pre- and post-groups, and no significant difference was observed between these groups. There were few apoptotic cell deaths in all groups. Compared to the control group, significantly fewer cell deaths by autophagy were found in the pre- and post-group. We concluded that silymarin exerts a preservation effect on delayed neuronal cell death in the rat hippocampus and this effect has nothing to do with the timing of administering of silymarin.