[Age-dependent expression of HSP90 in the hippocampus of APP/PS1 mice].

The present study aims to observe the change in expression of heat shock protein 90 (HSP90) along with amyloid-β (Aβ) and phosphorylated Tau (p-Tau) protein levels in the hippocampus tissue of Alzheimer's disease (AD) transgenic animal model with age. APP/PS1 transgenic mice at age of 6-, 9- and 12-month and C57BL/6J mice of the same age were used. The cognitive abilities of these animals were evaluated using a Morris water maze.

[Time dependent expression profiling of PTK2B and its relationship with Aβ, Tau and LRP-1 in hippocampus and blood of APPswe/PS1dE9 double-transgenic mouse].

To uncover the time-dependent expression pattern of gene and encoded protein, protein tyrosine kinase 2 beta(PTK2B), in the brain tissues of transgenic animal models of Alzheimer's disease (AD) and its relationship with the levels of Aβ phosphorylation of Tau (p-Tau) and low density lipoprotein receptor-related protein-1(LRP-1) in blood and brain tissues. In this study, 5-, 10- and 15-month-old APPswe/PS1dE9 double-transgenic mice harboring the genotype of AD confirmed by the gene test were divided into the 5-, 10- and 15-month-old experiment groups, and simultaneously, age-matched C57BL/6J mice were placed into the corresponding control groups, with 8 mice in each group. All mice were subjected to the Morris Water Maze for test of cognitive and behavioral ability.

[PTK2B affects the levels of Aβ in blood and brain and behavioral functions via targeting LRP-1 transporter in Aβ-induced cognitive dysfunction mice].

The aim of the present study was to explore the correlation between ptk2b/PTK2B (protein tyrosine kinase 2 beta, a ptk2b-encoded protein) and the level of low density lipoprotein receptor-related protein-1 (LRP-1), as well as to uncover the relationship between the changes in beta amyloid protein (Aβ) levels in blood and brain and the expression of ptk2b in Aβ-induced cognitive dysfunction mice. A total of 64 3-month-old C57BL/6J mice were divided randomly into the experimental group and control group. All mice underwent the intracerebroventricular (i.

Histone deacetylase-6 modulates amyloid beta-induced cognitive dysfunction rats by regulating PTK2B.

The aim of this study was to investigate the effects of histone deacetylase-6 (HDAC6) on the functional and pathological changes of the amyloid beta (Aβ)-induced cognitive dysfunction rats by regulating protein tyrosine kinase 2 beta (PTK2B). Ninety Sprague Dawley rats were randomly divided into nine groups, consisting of five experimental groups and four control groups. In five experimental groups, Aβ1-42 was infused intracerebroventricularly and 3 days later, rats in each group were infused intracerebroventricularly with tubastatin A hydrochloride (TSA), the HDAC6-specific inhibitor (Aβ + TSA group), theophylline, the HDACs agonist (Aβ + Theo group), PF431396 (PF), the PTK2B inhibitor (Aβ + PF group), the combination of PF and theophylline (Aβ + PF + Theo group), and normal saline (Aβ + normal saline group), respectively.

Histone deacetyltase 6 modulates amyloid β-induced cognitive dysfunction rats by regulating protein tyrosine kinase 2 beta.

The aim of this study was to investigate the effects of histone deacetyltase (HDAC) 6 on the functional and pathological changes of the amyloid beta (Aβ)-induced cognitive dysfunction rats by regulating protein tyrosine kinase 2 beta (PTK2B). Ninety Sprague-Dawley rats were randomly divided into nine groups, consisting of five experimental groups and four control groups. In five experimental groups, Aβ1-42 was infused intracerebroventricularly and 3 days later, rats in each group were infused intracerebroventricularly with tubastatin A hydrochloride (TSA), the histone deacetyltase 6 (HDAC6)-specific inhibitor (Aβ + TSA group), theophylline, the HDACs agonist (Aβ + theophylline group), PF431396, the PTK2B inhibitor (Aβ + PF group), the combination of PF431396 and theophylline (Aβ + PF + theophylline group) and normal saline (Aβ + normal saline group), respectively.

[Temporal and spatial changes of α7nAChR and nNOS in cerebral cortex and hippocampus of Aβ-induced cognitive dysfunction rats].

The present study was to explore the temporal and spatial distributions and variations of α7 nicotinic acetylcholine receptor (α7nAChR) and neuronal nitric oxide synthetase (nNOS) in cerebral cortex and hippocampus of Aβ-induced cognitive dysfunction rats. Sixty Sprague-Dawley (SD) rats were randomly divided into six groups. Three experimental groups were intracerebroventricularly (i.

[The synergetic effects of nitric oxide and nicotinic acetylcholine receptor on learning and memory of rats].

The aim of the present study is to explore the interaction of nitric oxide (NO) and nicotinic acetylcholine receptor (nAChR) on learning and memory of rats. Rats were intracerebroventricularly (i.c.

Effects of L-arginine and N(ω)-nitro-L-arginine methylester on learning and memory and α7 nAChR expression in the prefrontal cortex and hippocampus of rats.

Nitric oxide (NO) is a novel type of neurotransmitter that is closely associated with synaptic plasticity, learning and memory. In the present study, we assessed the effects of L-arginine and N(ω)-nitro-L-arginine methylester (L-NAME, a nitric oxide synthase inhibitor) on learning and memory. Rats were assigned to three groups receiving intracerebroventricular injections of L-Arg (the NO precursor), L-NAME, or 0.

Effects of multiple intrathecal administration of L-arginine with different doses on formalin-induced nociceptive behavioral responses in rats.

Objective: To investigate the effects of nitric oxide (NO) with different doses on modulation of inflammatory pain, and its possible mechanisms.

Methods: NO precursor L-arginine (L-Arg) was intrathecally administered in rats at a dose of 10 microg per day (low dose group) or 250 microg per day (high dose group) for a succession of 4 d. Normal saline was applied as a control.

[Amplification and specific expression of T-bet gene in nasal NK/T cell lymphoma].

Objective: To investigate the specific genetic alterations in nasal NK/T cell lymphoma (N-NK/T-L) and the significance thereof.

Methods: Restriction landmark genomic scanning (RLGS) was performed on the specimen of a case of N-NK/T-L and the peripheral blood leukocytes of the same case. The RLGS image was analyzed with the Virtual genome scan (VGS) software so as to discover abnormality of T-bet gene.

[MK-801 suppresses dynorphin A (1-17)-induced facilitation of nociceptive responses to formalin in rats].

To explore the facilitation of nociceptive response by dynorphin (Dyn ) A in a model of formalin test in rats, the effects of single intrathecal injection (i.t.) of normal saline (NS), MK-801 (antagonist of NMDA receptor), naloxone (antagonist of opioid receptor), or Dyn A (1-17) were observed, and the effects of i.