Effects of 3′,4′-dihydroxyflavonol treatment on Neu N and BDNF and ICAM levels in the striatum of rats subjected to transient bilateral carotid occlusion-induced ischemia–reperfusion

Cerebral infarction is a leading cause of severe long-term disability and functional and cognitive impairment. With the advancement of acute stroke treatment, more patients are now experiencing stroke with varying degrees of impairment. The present study was conducted to determine the effects of 1-week 3,4-dihydroxyflavonol (DiOHF) administration during transient experimental cerebral ischemia-reperfusion (I/R) in rats on NeuN, Tuba1a, Tubb3, and calbindin were evaluated as markers of neuronal phenotype and cytoskeletal organization, while ICAM and BDNF were assessed in relation to inflammatory and neurotrophic processes. Changes in these markers indicate alterations in neuronal marker expression, cytoskeletal integrity, and neurotrophic and inflammatory status. In this study, a total of 28 male Wistar albino rats, aged 10-12 weeks and weighing 300-400 g, were used. 1-Control Group (n = 6): The animals in this group received no anaesthesia or surgical procedures. 2-Sham Group (n = 6): After general anaesthesia was induced in the animals in this group, the carotid artery regions were opened and closed. 3- Ischemia-Reperfusion Group (n = 8): Under general anaesthesia, the carotid arteries of the rats were isolated and ligated for 30 min, followed by ischemia. 4- Ischemia-Reperfusion + DiOHF Group (n = 8): Under general anaesthesia, the carotid arteries of the rats were ligated for 30 min, followed by ischemia. Reperfusion was then allowed. Tuba1A, Tubb3, ICAM and Calbindin were analyzed by real-time PCR, BDNF by a commercial ELISA kit, and NeuN by immunohistochemistry. I/R decreased the levels of Neu N, Tuba1a, Tubb3, calbindin and BDNF in the striatum tissues and increased ICAM levels. DiOHF supplementation halted the decrease in expression level in Tuba1a, Tubb3, Calbindin, BDNF; the Increase in Icam level.Also DiOHF supplementation prevented the decrease in the level of anti-NeuN antibody and led to an increase. The study results revealed that one week of transient I/R in rats suppressed NeuN, TUBA1A, TUBB3, calbindin and BDNF levels, which are important in neuronal phenotype and cytoskeletal organization inflammatory and neurotrophic processes. However, a week DiOHF treatment significantly corrected the distortions caused by I/R.