Abstract
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Highlights
● Hesperidin accelerates the BDNF-TrkB signaling pathway.
● Improved BDNF-TrkB signaling pathway can ameliorate neurodegenerative diseases.
● Hesperidin suppresses oxidative stress parameters in the fetal cerebral cortex of the UPI rat model.
● Hesperidin is effective in reducing cerebral cortex damage with its antioxidant role.
● Hesperidin can be effective in reducing UPI-induced cerebral cortex damage.
Plain Language Summary
The abnormal fetal growth etiology and its mechanism, i.e., Intrauterine Growth Restriction (IUGR), remain unclear. IUGR produces significant neurodevelopmental deficits affecting the IUGR offspring’s cerebral cortex. Furthermore, compounds, including Hesperidin (Hes) (of different antimicrobial & antioxidant properties) might present neuroprotective effects. In this study, initially, the UPI model was created by bilateral uterine vessel ligation, then the study rats were given oral Hes. Hes caused uterine and embryo weight gain in the UPI model. Analyzing antioxidant parameters suggested that the Catalase (CAT) activity and Total Antioxidant Capacity (TAC) increased, and Malondialdehyde (MDA) decreased after Hes administration in the fetal cerebral cortex. BDNF plays a crucial role in brain development, including neural migration, neurogenesis, and synapse formation in the antenatal and postnatal. Hesperidin also increased BDNF and its receptor, TrkB, in the UPI model. In general, the collected results indicated that Hes could effectively reduce the IUGR-induced cerebral cortex damage. Additionally, Hes may provide the beneficial therapeutic potential to inhibit and treat the neurodegenerative disorders associated with intrauterine growth restriction.