Annals of Medical Research, cilt.30, sa.2, ss.175-182, 2023 (Hakemli Dergi)
Aim: Due to the loss of neurons and neural network functions in the brain, cerebral ischemia is the leading cause of permanent disability in adults all over the world. An- tioxidants scavenge free radicals and protect tissues against oxidative damage caused by ischemia/reperfusion. This study aims to investigate the protective effects of myricetin, a powerful antioxidant, against cerebral ischemia/reperfusion injury. Materials and Methods: There were 5 experimental groups in this study; control, sham, ischemia/reperfusion (I/R), Myricetin 3 (Myr 3), and Myricetin 6 (Myr 6), and 8 rats in each group. Four-vessel occlusion was made to create ischemia. The ischemia and subsequent reperfusion period were 30 minutes each. One hour before ischemia, 3 mg/kg of myricetin was given to rats in the Myr 3 group and 6 mg/kg of myricetin was given to rats in the Myr 6 group. GolgiCox and Caspase3 stainings were carried, SOD, and MDA levels were investigated, and TNF-α mRNA expression levels were measured in brain tissue. Results: This study’s results showed that; the number of neurons decreased drastically in the CA1region of the hippocampus in the I/R group. Distance between cells increased, and the neurons were spaced apart and randomly distributed. Neuronal loss in the hip- pocampus was reduced and the amounts of neurons rise in the Myr 3 group compared to the I/R group. A significant decrease was detected in the SOD values of the I/R group. Compared to the I/R group, the SOD values of Myr 3 and Myr 6 groups increased sig- nificantly. MDA level of the I/R group increased significantly compared to the control. MDA values of Myr 3 and Myr 6 groups decreased significantly when compared to the I/R group. TNF-α mRNA expression level was significantly higher in the I/R group. A significant reduction was observed in the mRNA expression level in the Myr 3 group. Conclusion: In conclusion, the findings of this study suggest that myricetin is a promising agent for inhibiting the ischemia-induced cerebral inflammatory response and oxidative stress.