Farnaz Nikbakht
Iran University of Medical Sciences, Iran
Title: Amelioration of mitochondrial dysfunction and hippocampal neuronal death by Apigenin in an Alzheimer’s disease model
Biography
Biography: Farnaz Nikbakht
Abstract
Background & Purpose: Apigenin, a non-toxic and non-mutagenic flavone, has the potential of free radical scavenging activity. Recent studies revealed the protective effect of apigenin against Aβ neurotoxicity but the underlying mechanism was unclear. The purpose of this study was to reveal the protective effect of apigenin against Aβ 25-35 by inhibition of mitochondrial caspase 9 and cytochrome C release. The ability of apigenin to prevent dynamin-related protein (Drp1) activation and thereby protection against mitochondrial fragmentation and dysfunction was the second goal of this study.
Methods: Aβ 25-35 was microinjected into the left lateral cerebral ventricle. Oral administration of apigenin was started half an hour before the surgery and continued for the following 21 days. After three weeks, the animals were sacrificed and their brains were removed for further histological and molecular processes. Cell death and neurodegeneration was assessed by Nissl and Fluoro Jade B staining in CA1 area of the hippocampus. Cytochrome C and caspase 9 was detected by immunohistochemistry in the same area and Drp1 was detected by western blotting.
Results: The results revealed that oral administration of apigenin protected CA1 neurons from Aβ toxicity (P<0.001 for Nissl and Fluoro Jade B). The protection was associated with a significant decrease in mitochondrial caspase 9 and Cytochrome C release (P<0.01). Drp1 was also significantly decreased in apigenin treated groups (P<0.01).
Conclusion: These data demonstrate that the flavone apigenin protects highly vulnerable CA1 neurons against Aβ toxicity and suggest that it is mediated by amelioration in mitochondrial dysfunction.