Protective Effects of Baicalin on Aβ1–42-Induced Learning and Memory Deficit, Oxidative Stress, and Apoptosis in Rat

• Published in: Cellular and molecular neurobiology Vol. 35; no. 5; pp. 623 - 632
• Main Authors: Ding, Haitao, Wang, Haitao, Zhao, Yexia, Sun, Deke, Zhai, Xu
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.07.2015
• Subjects: Amyloid beta-Peptides - toxicity; Animals; Antioxidants - metabolism; Apoptosis - drug effects; bcl-2-Associated X Protein - metabolism; Biomedical and Life Sciences; Biomedicine; Caspases - metabolism; Cell Biology; Cell Nucleus - drug effects; Cell Nucleus - metabolism; Cytochromes c - metabolism; Enzyme Activation - drug effects; Flavonoids - chemistry; Flavonoids - pharmacology; Flavonoids - therapeutic use; Hippocampus - drug effects; Hippocampus - pathology; Male; Malondialdehyde - metabolism; Membrane Potential, Mitochondrial - drug effects; Memory Disorders - drug therapy; Memory Disorders - pathology; Neurobiology; Neuroprotective Agents - chemistry; Neuroprotective Agents - pharmacology; Neuroprotective Agents - therapeutic use; Neurosciences; NF-E2-Related Factor 2 - metabolism; Original Research; Oxidative Stress - drug effects; Rats, Wistar; Real-Time Polymerase Chain Reaction; Aβ; Oxidative stress; Learning and memory deficit; Alzheimer’s disease; Baicalin; Apoptosis
• ISSN: 0272-4340; 1573-6830
• DOI: 10.1007/s10571-015-0156-z

The accumulation and deposition of β-amyloid peptide (Aβ) in senile plaques and cerebral vasculature is believed to facilitate the progressive neurodegeneration that occurs in the Alzheimer’s disease (AD). The present study sought to elucidate possible effects of baicalin, a natural phytochemical, on Aβ toxicity in a rat model of AD. By morris water maze test, Aβ 1–42 injection was found to cause learning and memory deficit in rat, which was effectively improved by baicalin treatment. Besides, histological examination showed that baicalin could attenuate the hippocampus injury caused by Aβ. The neurotoxicity mechanism of Aβ is associated with oxidative stress and apoptosis, as revealed by increased malonaldehyde generation and TUNEL-positive cells. Baicalin treatment was able to increase antioxidant capabilities by recovering activities of antioxidant enzymes (superoxide dismutase, catalase, and glutathione peroxidase) and up-regulating their gene expression. Moreover, baicalin effectively prevented Aβ-induced mitochondrial membrane potential decrease, Bax/Bcl-2 ratio increase, cytochrome c release, and caspase-9/-3 activation. In addition, we found that the anti-oxidative effect of baicalin was associated with Nrf2 activation. In conclusion, baicalin effectively improved Aβ-induced learning and memory deficit, hippocampus injury, and neuron apoptosis, making it a promising drug to preventive interventions for AD.