Catalpol increases hippocampal neuroplasticity and up-regulates PKC and BDNF in the aged rats.
Rehmannia, a traditional Chinese medical herb, has a long history in age-related disease therapy. Previous work has indicated that catalpol is a main active ingredient performing neuroprotective effect in rehmannia, while the mechanism underlying the effect remains poorly understood. In this study, we attempt to investigate the effect of catalpol on presynaptic proteins and explore a potential mechanism. The hippocampal levels of GAP-43 and synaptophysin in 3 groups of 4 months (young group), 22-24 months (aged group) and catalpol-treated 22-24 months (catalpol-treated group) rats were evaluated by western blotting. Results clearly showed a significant decrease in synaptophysin (46.6%) and GAP-43 (61.4%) levels in the aged group against the young animals and an increase (45.0% and 31.8% respectively) in the catalpol-treated aged rats in comparison with the untreated aged group. In particular, synaptophysin immunoreactivity (OD) in the dentate granule layer of the hippocampus was increased 0.0251 in the catalpol-treated group as compared with the aged group. The study also revealed a catalpol-associated increase of PKC and BDNF in the hippocampus of the catalpol-treated group in comparison with the aged rats and highly correlated with synaptophysin and GAP-43. Such positive correlations between presynaptic proteins and signaling molecules also existed in the young group. These results suggested that catalpol could increase presynaptic proteins and up-regulate relative signaling molecules in the hippocampus of the aged rats. Consequently, it seemed to indicate that catalpol might ameliorate age-related neuroplasticity loss by "normalizing" presynaptic proteins and their relative signaling pathways in the aged rats.
Liu
Jing
J
Department of Bioscience and Biotechnology, School of Environmental and Biological Sciences, Dalian University of Technology, 2 Linggong Road, Dalian, Liaoning 116024, PR China.
He
Qiao-Jie
QJ
Zou
Wei
W
Wang
Hong-Xia
HX
Bao
Yong-Ming
YM
Liu
Yu-Xin
YX
An
Li-Jia
LJ
D000375:Aging / Q000187:drug effects / Q000378:metabolism*; D000704:Analysis of Variance; D000818:Animals; D019208:Brain-Derived Neurotrophic Factor / Q000187:drug effects* / Q000378:metabolism; D004365:Drugs, Chinese Herbal / Q000494:pharmacology; D019922:GAP-43 Protein / Q000187:drug effects / Q000378:metabolism; D005960:Glucosides / Q000494:pharmacology*; D006624:Hippocampus / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D057888:Iridoid Glucosides; D039823:Iridoids / Q000494:pharmacology*; D008297:Male; D009473:Neuronal Plasticity / Q000187:drug effects*; D018696:Neuroprotective Agents / Q000494:pharmacology; D011493:Protein Kinase C / Q000187:drug effects* / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D018709:Statistics, Nonparametric; D016708:Synaptophysin / Q000187:drug effects / Q000378:metabolism; D015854:Up-Regulation
D019208:Brain-Derived Neurotrophic Factor; D004365:Drugs, Chinese Herbal; D019922:GAP-43 Protein; D005960:Glucosides; D057888:Iridoid Glucosides; D039823:Iridoids; D018696:Neuroprotective Agents; D016708:Synaptophysin; C078040:catalpol; D011493:Protein Kinase C