Myricetin Ameliorates Brain Damage Induces by Cerebral Ischemia-Reperfusion Injury in Rats
الباحث الأول:
Laith M Abbas Al-Husein
الباحثين الآخرين:
Wadhah Mahbuba, Manar Hameed Mohammed, Fadhaa Abdulameer Ghafil, Maysaa Ali Abdul Khaleq, Najah R Hadi, Zina Zwaini
المجلة:
Asian Journal of Pharmaceutics
تاريخ النشر:
None
مختصر البحث:
Interruption of blood flow may result in considerable tissue damage via ischemia/reperfusion injury induced oxidative stress in brain tissues. The present study aimed to investigate the effects of myricetin treatment in rats cerebral I/R injury.
M…
Interruption of blood flow may result in considerable tissue damage via ischemia/reperfusion injury induced oxidative stress in brain tissues. The present study aimed to investigate the effects of myricetin treatment in rats cerebral I/R injury.
Material and Methods:
The study was carried out on 36 Wistar-albino rats, divided into four groups including Sham group, I/R group, I/R+(control-vehicle DMSO) and I/R+ myricetin 50 mg/kg intraperitoneally 1 hour before induction of ischemia. Measurement of brain tissue IL-1β, ICAM-1, caspase-3, Notch 1 and jagged 1 was done after one hour of reperfusion with assessment of the brain infarcted area and histopathological analysis.
Results:
Myricetin attenuates the cerebral I/R injury induced increase in inflammatory cytokine (IL-1β), adhesion molecule (ICAM-1) and proapoptotic enzyme (caspase-3). Additionally, it reduces the size of infarcted area and histopathological damage. However, such protective effect was not found to be mediated by Notch 1 pathway because myricetin treatment didn’t show changes in the increased levels of Notch 1 and Jagged 1 seen in brain with I/R injury.
Conclusions:
Myricetin has a neurocytoprotective effect against cerebral I/R injury which is manifested as anti-inflammatory anti-apoptotic preserving cell structure and viability, nevertheless this effect is not mediated through Notch 1 pathway.
