Mechanism of tau hyperphosphorylation in brain cortex of diabetic rats and effect of LiCl / 中国医学科学院学报

<p><b>OBJECTIVE</b>To 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.</p><p><b>METHODS</b>The 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.</p><p><b>RESULTS</b>Compared 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).</p><p><b>CONCLUSION</b>The 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.</p>

Alteration of beta-amyloid and glutamate transporter in the brain of diabetes rats and the underlying mechanism / 中国医学科学院学报

<p><b>OBJECTIVE</b>To investigate the alteration of beta-amyloid (Abeta) and glutamate transporter in the brain cortex of diabetes mellitus (DM) rats and the underlying mechanism.</p><p><b>METHODS</b>The 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) and the function of glutamate transporter were measured by 32P-labelling. The amount of Abeta was determined by enzyme-linked immunosorbentassay.</p><p><b>RESULTS</b>In DM group, the level of Abeta40 increased (P < 0.01), but the function of glutamate transporter was impaired (P < 0.05). The activity of GSK-3 was stimulated (P < 0.05). Compared with DM group, the level of Abeta40 was restored (P < 0.01), and the function of glutamate transporter was enhanced (P < 0.05) in LiCl treated group, accompanied by a decreased activity of GSK-3.</p><p><b>CONCLUSION</b>Overproduction of Abeta and impaired glutamate transporter exist in DM rats, and increase of GSK-3 may play a crucial role in this process.</p>

The role of angiotension II receptor and calpain in myocardium remodeling / 中国应用生理学杂志

<p><b>AIM</b>To investigate the relation among myocardial angiotension II receptor (AT1/AT2) expression, calpain and cardiac function in patients with congestive heart failure (CHF).</p><p><b>METHODS</b>Message RNA (mRNA) expression of AT1/AT2 receptor in myocardial tissue of 39 patients with CHF due to valvular heart disease and 8 control subjects were analyzed using reverse transcriptase-polymerase chain reaction (RT-PCR). Immunoprecipitation was used to assay the protein expression of u-calpain and m-calpain.</p><p><b>RESULTS</b>Pathological changes of myocardial tissue in CHF due to valvular heart disease showed typical myocardial remodeling. AT1 receptor mRNA expression was slightly increased in the patients with mild CHF than in the control subjects, but decreased in the moderate and severe CHF patients. No difference was observed in AT2 receptor mRNA expression among all the groups, but the ratio of AT1/AT2 decreased. The protein expression of u-calpain and m-calpain were positively correlated to the levels of cardiac function in patient with CHD.</p><p><b>CONCLUSION</b>The expression of AT1 receptor is down-regulated in moderate and severe CHF, the dominant receptor subtype is transformed to AT2. Cardiomyocyte apoptosis or death may be induced via AT2 receptor to activate calpain system, leading the deterioration of cardiac function.</p>