Protective effects of luteolin against cognitive impairment induced by infusion of Aβ peptide in rats.
Luteolin can be found in many traditional Chinese medicines, it's a falconoid compound derived from Lonicera japonica Thunb. This study aims to investigate the neuroprotective effects of luteolin against cognitive impairment induced by amyloid-β (Aβ) peptide and the underlying mechanisms in rats. The animal behavioral tests showed that luteolin could ameliorate Aβ-induced learning and memory impairment. In hippocampal tissue, the activity of choline acetyl transferase (ChAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) increased after treated by luteolin. Luteolin also reversed the increased activity of acetylcholine esterase (AchE). In hippocampi homogenate, the content of acetylcholine (Ach) increased, but malondialdehyde (MDA) reduced. Moreover, luteolin can increase Bcl-2/Bax ratio. This study demonstrated that luteolin could protect Alzheimer's disease (AD) rats against Aβ-induced cognitive impairment through regulating the cholinergic system and inhibiting oxidative injuries. The results suggesting that luteolin may have potential as a therapy for AD.
Department of Neurology, Yantaishan Hospital Yantai 264000, China.
Tian-Xia
TX
Yu
Department of Neurology, Yeda Hospital Yantai 264000, China.
Peng
P
Zhang
Department of Oncology, Shandong Province Tumor Hospital Jinan 250000, China.
Yan
Y
Guan
Department of Neurology, Yantaishan Hospital Yantai 264000, China.
Min
M
Wang
Department of Neurology, Yeda Hospital Yantai 264000, China.
Ming-Qing
MQ
Zhen
D000110:Acetylcholinesterase / Q000378:metabolism; D016229:Amyloid beta-Peptides; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001522:Behavior, Animal / Q000187:drug effects*; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D003071:Cognition / Q000187:drug effects*; D003072:Cognition Disorders / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control* / Q000523:psychology; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D058851:GPI-Linked Proteins / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006624:Hippocampus / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D047311:Luteolin / Q000494:pharmacology*; D008315:Malondialdehyde / Q000378:metabolism; D018782:Maze Learning / Q000187:drug effects; D008568:Memory / Q000187:drug effects; D018696:Neuroprotective Agents / Q000494:pharmacology*; D018384:Oxidative Stress / Q000187:drug effects; D010446:Peptide Fragments; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000378:metabolism
D016229:Amyloid beta-Peptides; D000975:Antioxidants; C494828:Bax protein, rat; D058851:GPI-Linked Proteins; D018696:Neuroprotective Agents; D010446:Peptide Fragments; D019253:Proto-Oncogene Proteins c-bcl-2; C078592:amyloid beta-protein (1-40); D051028:bcl-2-Associated X Protein; D008315:Malondialdehyde; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D002795:Choline O-Acetyltransferase; D000110:Acetylcholinesterase; C548246:Ache protein, rat; D047311:Luteolin
Alzheimer’s disease; Aβ peptide; Luteolin; antioxidant activity; neuroprotection