[Protective effect of oligosaccharides from Morinda officinalis on beta-amyloid-induced dementia rats].
OBJECTIVE
To observe the effect of oligosaccharides of Morinda officinalis (OMO) on beta-amyloid-induced dementia rats, and study its pharmacological mechanism in treatment of dementia.


METHODS
The dementia model rats were established by injecting Abeta25-35 10 microLg into bilateral hippocampus. OMO high-dose (60 mg . kg-1 . d-1) group, OMO low-dose (20 mg . kg-1 . d-1 ) groups, the blank group, the sham operation group and the positive donepezil HC1 group (0. 125 mg kg-1 . d-1) were designed for the experiment. They were continuously administered with drugs at the 15th day after operation for 25 days. Kit microplate method was used to detect the contents of super oxide dismutase (SOD), malondialdehyde (MDA), catalase (CAT), glutathione reductase (GSH-Px), acetylcholine (ACh) , acetylcholinesterase (AChE) and Na+ /K+ -ATPase.


RESULTS
Compared with the model group, all of administration groups showed higher SOD, CAT and GSH-Px levels, and lower MDA in the brain tissues. Besides, they also showed rise in the activities of ACh and Na+ /K+ -ATPase.


CONCLUSIONS
OMO can ameliorate on beta-amyloid-induced dementia rats by enhancing oxidation resistance, activating brain energy metabolism and improving the injury of cholinergic system.
Pharmaceutical Research Institute, South China Normal University, Guangzhou 510631, China. diling0828@sina.com
Di-Ling
DL
Chen
Peng
P
Zhang
Li
L
Lin
He-Ming
HM
Zhang
Song-Hao
SH
Liu
D000110:Acetylcholinesterase / Q000378:metabolism; D016229:Amyloid beta-Peptides / Q000633:toxicity*; D000818:Animals; D002374:Catalase / Q000378:metabolism; D003704:Dementia / Q000139:chemically induced* / Q000188:drug therapy*; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D032066:Morinda / Q000737:chemistry*; D018696:Neuroprotective Agents / Q000378:metabolism; D009844:Oligosaccharides / Q000627:therapeutic use*; D018384:Oxidative Stress / Q000187:drug effects; D010446:Peptide Fragments / Q000633:toxicity*; D051381:Rats; D013482:Superoxide Dismutase / Q000378:metabolism
D016229:Amyloid beta-Peptides; D018696:Neuroprotective Agents; D009844:Oligosaccharides; D010446:Peptide Fragments; C074636:amyloid beta-protein (25-35); D008315:Malondialdehyde; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D000110:Acetylcholinesterase