POLYDATIN, A HERBAL BIOFLAVONOID, IS PROTECTIVE AGAINST CEREBRAL ISCHEMIA-REPERFUSION INJURY: MOLECULAR, BIOCHEMICAL AND HISTOLOGICAL DATA

POLYDATIN, A HERBAL BIOFLAVONOID, IS PROTECTIVE AGAINST CEREBRAL ISCHEMIA-REPERFUSION INJURY: MOLECULAR, BIOCHEMICAL AND HISTOLOGICAL DATA

This study aims to research the protective effects Polydatin have against cerebral ischemia/reperfusion damage. Polydatin is a natural polyphenic phytoalexin and which has strong antioxidant properties. In the present study, 5 groups were prepared as control, sham, ischemia/reperfusion (IR), Polydatin 30 (Pol 30), and Polydatin 60 (Pol 60). The four-vessel occlusion model was used to induce ischemia. Polydatin was injected intraperitoneally 30 minutes before ischemia. Hematoxylin Eosin staining were applied for histopathological study, SOD, CAT, and MDA levels determined, and TNF-α mRNA expression levels were measured by the RT-qPCR technique in brain tissue. According to the results, a serious loss of neurons in the CA 1 region of the hippocampus was observed in the IR group. Neuronal damage in the hippocampus decreased and the number of neurons increased significantly in the Pol 60 group compared to the IR group. CAT and SOD levels were reduced, and the MDA level rose in the IR group. In Pol 60 and Pol 30 groups, an increase was observed in the CAT and SOD levels, a decrease was observed in the MDA and total protein levels compared to the IR group. The amount of TNF-α mRNA expression in the brain tissues of the IR group was significantly higher compared to the control group. In the Pol 60 group, mRNA expression level decreased significantly compared to the IR group. In conclusion, the increase in MDA, decrease in SOD and CAT values, increase in TNF-α gene mRNA expression, and histological damage in the brain because of cerebral ischemia/reperfusion in rats were restored to normal levels with 30 and 60 mg/kg polydatin administration as protective before ischemia. Especially at 60 mg/kg polydatin supplementation with antioxidant properties has a neuroprotective effect against oxidative stress damage caused by cerebral ischemia/reperfusion.

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Journal of Scientific Reports-A-Cover
  • Başlangıç: 2020
  • Yayıncı: Kütahya Dumlupınar Üniversitesi