Neuroprotective effects of Tongmai Yizhi Decoction () against Alzheimer's disease through attenuating cyclin-dependent kinase-5 expression.
- Author:
Jing-Han FENG
1
;
Bao-Chang CAI
2
;
Wei-Feng GUO
3
;
Ming-Yan WANG
4
;
Yong MA
1
;
Qiao-Xi LU
1
Author Information
- Publication Type:Journal Article
- Keywords: Alzheimer's disease; Chinese medicine; Tongmai Yizhi Decoction; cyclin-dependent kinase-5
- MeSH: Alzheimer Disease; drug therapy; pathology; Animals; Cognition; drug effects; Cyclin-Dependent Kinase 5; metabolism; Disease Models, Animal; Down-Regulation; drug effects; Drugs, Chinese Herbal; therapeutic use; Female; Hippocampus; drug effects; Male; Maze Learning; drug effects; Memory; drug effects; Neuroprotective Agents; therapeutic use; Rats; Rats, Sprague-Dawley
- From: Chinese journal of integrative medicine 2017;23(2):132-137
- CountryChina
- Language:English
-
Abstract:
OBJECTIVESTo explore the protective effects of Tongmai Yizhi Decoction (, TYD), a Chinese herb complex prescription against the impairment of cognitive functions and memory loss in amyloid beta 1-40 (Aβ) peptide and ibotenic (IBO)-induced Alzheimer's disease (AD) model rats.
METHODSThe in vivo model was established by injecting Aβand IBO into left hippocampal CA1 area of Sprague-Dawley (SD) rat to mimic AD. Totally 32 SD rats were divided into 4 groups, including sham operation group, AD model group, TYD group [AD rats treated with TYD at the dosage of 19.44 g/(kg•d) for 4 weeks] and huperzine A group [AD rats treated with huperzine A at the dosage of 40.5 μg/(kg•d) for 4 weeks]. Spatial learning and memory level was detected by Morris Water Maze test. Histological morphology in the hippocampus was tested by hematoxylin-eosin (HE) staining. Cyclin-dependent kinase-5 (Cdk5) protein and gene expression level were investigated by Western blot analysis and real-time quantitative polymerase chain reaction (RT-qPCR), respectively.
RESULTSAβ1-40 and IBO treatment induced longer escape latency of rats, compared with sham operation group from day 25 (P<0.01). However, TYD and huperzine A obviously shortened the escape latency from day 26 (P<0.01). Moreover, the effect of TYD was similar to huperzine A (P>0.05). Furthermore, HE staining also showed that TYD and huperzine A reversed the neuropathological changes in the hippocampus triggered by Aβ1-40 and IBO. TYD and huperzine A effectively reduced the expression levels of Cdk5 protein and gene located in rat hippocampus, compared with the AD model group (P<0.01).
CONCLUSIONTYD could be a promising neuroprotective agent for protecting neuron from AD injury through inhibiting Cdk5 expression.
