Green tea polyphenols protect against okadaic acid-induced acute learning and memory impairments in rats.
OBJECTIVE
Green tea polyphenols (GTPs) are now being considered possible protective agents in neurodegenerative diseases such as Alzheimer's disease (AD). Previous studies suggested that GTPs could inhibit amyloid fibril formation and protect neurons from toxicity induced by β-amyloid. However, whether GTPs can ameliorate learning and memory impairments and also reduce tau hyperphosphorylation induced by okadaic acid (OA) in rats remains unclear. The aim of this study was to determine if GTPs have neuroprotection against OA-induced neurotoxicity.


METHODS
In this work, rats were pretreated with GTPs by intragastric administration for 4 wk. Then OA was microinjected into the right dorsal hippocampus. Morris water maze tests were used to test the ethologic changes in all groups, and tau protein hyperphosphorylation was detected both in vivo and in vitro.


RESULTS
The ethologic test indicated that the staying time and swimming distance in the target quadrant were significantly decreased after OA treatment, whereas rats pretreated with GTPs stayed longer in the target quadrant. Methyl thiazolyl tetrazolium assay and lactate dehydrogenase leakage showed that GTPs greatly ameliorated primary hippocampal neurons damage induced by OA. Furthermore, reduced hyperphosphorylated tau protein was detected with GTPs pretreatment.


CONCLUSIONS
Taken together, our results suggest that GTPs have neuroprotection against OA-induced neurotoxicity.
Department of Physiology, Dalian Medical University, Dalian, China.
Hongyu
H
Li
Department of Physiology, Dalian Medical University, Dalian, China.
Xiukui
X
Wu
Department of Physiology, Dalian Medical University, Dalian, China.
Qiong
Q
Wu
Department of Physiology, Dalian Medical University, Dalian, China.
Dezheng
D
Gong
Department of Physiology, Dalian Medical University, Dalian, China.
Meijun
M
Shi
Department of Physiology, Dalian Medical University, Dalian, China.
Lili
L
Guan
Department of Physiology, Dalian Medical University, Dalian, China.
Jun
J
Zhang
Department of Physiology, Dalian Medical University, Dalian, China.
Jing
J
Liu
Department of Physiology, Dalian Medical University, Dalian, China.
Bo
B
Yuan
Faculty of Pharmacology, Dalian Medical University, Dalian, China.
Guozhu
G
Han
Department of Physiology, Dalian Medical University, Dalian, China. Electronic address: zouyuan@hotmail.com.
Yuan
Y
Zou
D000544:Alzheimer Disease; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism; D007858:Learning / Q000187:drug effects*; D018782:Maze Learning; D008569:Memory Disorders / Q000139:chemically induced / Q000188:drug therapy*; D018696:Neuroprotective Agents / Q000494:pharmacology*; D019319:Okadaic Acid / Q000008:administration & dosage / Q000009:adverse effects*; D010766:Phosphorylation / Q000187:drug effects; D059808:Polyphenols / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013662:Tea / Q000737:chemistry*; D016875:tau Proteins / Q000235:genetics / Q000378:metabolism
D000975:Antioxidants; C489131:Mapt protein, rat; D018696:Neuroprotective Agents; D059808:Polyphenols; D013662:Tea; D016875:tau Proteins; D019319:Okadaic Acid
Green tea polyphenols; Hyperphosphorylation; Neuroprotection; Okadaic acid; Tau protein