Mechanism of tau hyperphosphorylation in brain cortex of diabetic rats and effect of LiCl.
- Author:
Zhong-sen QU
1
;
Qing TIAN
;
Xin-wen ZHOU
;
Qun WANG
;
Qi ZHANG
;
Jian-zhi WANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cerebral Cortex; metabolism; Diabetes Mellitus, Experimental; complications; Glycogen Synthase Kinase 3; metabolism; Lithium Chloride; therapeutic use; Male; Memory Disorders; drug therapy; metabolism; Phosphorylation; drug effects; Rats; Rats, Sprague-Dawley; tau Proteins; metabolism
- From: Acta Academiae Medicinae Sinicae 2006;28(2):244-248
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the mechanism of tau hyperphosphorylation and the effect of LiCl on tau phosphorylation and the memory retention deficits in streptozotocin-induced diabetes mellitus (DM) rats.
METHODSThe rats were randomly divided into control, DM, DM + NaCl, and DM + LiCl groups and diabetes was induced by streptozotocin. The activity of glycogen synthase kinase-3 (GSK-3) was measured by 32P-labelling. The level of tau phosphorylated and changes of memory retention were examined by Western blotting and step down test, respectively.
RESULTSCompared with control group, the activity of GSK-3 and tau phosphorylation was increased, and the memory retention was impaired in DM group. When the rats were treated with LiCl, the activity of GSK-3 and hyperphosphorylation of tau were significantly arrested (P < 0.05, P < 0.01), and the memory retention deficit was significantly improved (P < 0.05).
CONCLUSIONThe hyperphosphorylation of tau can be induced by activation of GSK-3 in diabetic rats. Lithium protects tau from hyperphosphorylation and may rescue memory retention in the rats by inhibiting GSK-3 activity.
