This study investigates the neuroprotective effects of thalidomide (THA) in cerebral ischemia-reperfusion (I/R) injury induced by bilateral carotid artery occlusion in rats. Thirty-two female Wistar albino rats were divided into four groups: Sham, I/R, THA+I/R, and I/R+THA. I/R injury was induced by occluding both carotid arteries for 15 minutes followed by 24-hour reperfusion. THA (20 mg/kg) was administered intraperitoneally either before or after ischemia. Biochemical analyses measured malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and reduced glutathione (GSH) in brain tissues. Histopathological evaluations assessed neuronal degeneration and tissue damage. The I/R group exhibited significantly increased MDA levels and reduced SOD and GSH enzyme activities in cerebrum and cerebellum tissues (P < 0.05). THA treatment significantly decreased MDA levels and restored SOD and GSH enzyme activities in both THA+I/R and I/R+THA groups (P < 0.05). Histopathological analyses revealed neuronal degeneration in the I/R group, whereas THA treatment mitigated neuronal damage, particularly in the I/R+THA group. In the IR+THA group, there was a significant decrease in the severity of caspase-3 immunoreactivity compared to the I/R group. THA demonstrates neuroprotective effects against cerebral I/R injury by reducing oxidative stress and neuronal damage. Administration of THA post-ischemia appears to be more effective in preserving neuronal integrity. These findings suggest that THA has neuroprotective potential in an experimental model of cerebral I/R injury; however, given its known adverse effects, further studies focusing on safety, dosing, and risk-benefit balance are required before any clinical implications can be considered.
Ozhan et al. (Thu,) studied this question.