ArticleJournal of bioenergetics and biomembranes2026
Neuroprotective effect of 3',4'-dihydroxyflavonol on blood-brain barrier ıntegrity and matrix remodeling in rats with transient bilateral carotid occlusion-ınduced ıschemia-reperfusion.
Article in Journal of bioenergetics and biomembranes, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The reduced blood flow and energy substrates to the affected area during ischemia and sudden exposure to these molecules after ischemia is called reperfusion. Reperfusion can be as damaging to cells and tissues as ischemia. This study aims to examine the effects of brain Ischemia-Reperfusion (I/R) and 1-week 3',4'-Dihydroxyflavonol (DiOHF) treatment on Matrix Metalloproteinasease (MMP), occludin, claudin-5, and β-actin levels in frontal cortex and hippocampus tissue in male rats. In this study, twenty-eight male Wistar-Albino rats were allocated into four experimental groups: Control, Sham, Ischemia-Reperfusion (I/R), and Ischemia-Reperfusion + DiOHF. Under general anesthesia, bilateral carotid artery ligation was performed to induce ischemia for 30 min, followed by reperfusion. DiOHF supplementation (10 mg/kg) was administered for one week. At the end of the treatment period, the animals were sacrificed under general anesthesia, and the frontal cortex and hippocampus tissues were harvested. Gene expression levels of MMP-3, MMP-9, occludin, claudin-5, and β-actin in the collected tissues were analyzed using real-time PCR. While I/R suppressed the levels of claudin-5 and occludin in the frontal cortex and hippocampus, it increased the levels of β-actin, matrix metalloproteinase-3 (MMP-3), and matrix metalloproteinase-9 (MMP-9). 3',4'-Dihydroxyflavonol supplementation for 1 week corrected the deteriorations caused by I/R. The study results show that 1 week of 3',4'-Dihydroxyflavonol treatment after I/R corrects the changes in structural damage indicators caused by transient bilateral carotid occlusion-induced ischemia-reperfusion in the frontal cortex and hippocampus to a certain extent.
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