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, Aβ 1–42 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. Rats in four control groups took normal saline that was equivalent to the volume of Aβ 1–42 , and 3 days later, TSA group, theophylline group, PF431396 (PF group), or normal saline group was given at a volume of 5 µL for rats in each group. Our results showed that HDAC6 may not only lead to the deterioration of learning and memory abilities but also elevate the levels of Aβo and Tau phosphorylation in Aβ-induced cognitive dysfunction rats via up-regulating PTK2B.
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