Molecular medicine reports
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Attention-deficit hyperactivity disorder (ADHD) is a neurobehavioral disorder characterized by inattention, hyperactivity and impulsivity. In the present study, we investigated the effects of swimming exercise on the symptoms of ADHD in correlation with the expression levels of dopamine and the dopamine D2 receptor. Adult male spontaneous hypertensive rats (SHRs) were used as animal models of ADHD and Wistar-Kyoto rats were used as controls. ⋯ The expression levels of TH and the dopamine D2 receptor were decreased and increased in ADHD rats, respectively, when compared with control rats. Swimming exercise enhanced the expression of TH and suppressed the expression of the dopamine D2 receptor in ADHD rats. In the present study, swimming exercise improved the symptoms of ADHD by upregulating the expression of dopamine and downregulating the expression of the dopamine D2 receptor.
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Gap junctions (GJs) enhance the cytotoxicity of specific cancer chemotherapeutic drugs and therefore, the inhibition of functional GJs may represent a mechanism by which the toxicity of chemotherapeutics in cancer cells can be reduced. In the present study, the effects and mechanisms of paclitaxel and docetaxel on GJ intercellular communication (GJIC) and the modulation of drug cytotoxicity were investigated in HeLa cells that were stably transfected with the connexin (Cx) 32 expression plasmid. Paclitaxel, but not docetaxel, was observed to inhibit dye‑coupling through junctional channels. ⋯ In addition, paclitaxel‑induced downregulation of GJIC decreased the cytotoxicity of paclitaxel in the presence of functional GJs compared with that of docetaxel, which did not affect Cx32 channels. These observations demonstrated that the differential effects of paclitaxel and docetaxel on GJIC may affect the cytotoxicity of chemotherapeutic drugs. The present study provides a promising new approach to select antineoplastics and improve drug efficacy in carcinoma cells that form GJs.
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The aim of the present study was to uncover the mechanism underlying the neuroprotection of Hemin‑mediated neuroglobin (Ngb) in an in vivo model of brain injury. Sixty healthy male Sprague-Dawley rats were randomly divided into 5 groups (n=12, each group): sham surgery, ischemia, Hemin, LY294002 (LY) and Hemin + LY. Focal cerebral ischemia was established by unilateral middle cerebral artery occlusion. ⋯ By contrast, LY treatment increased infarct volume, deteriorated neurological functions and significantly reduced expression of pAkt; however, Ngb mRNA and protein expression was unchanged. When compared with Hemin alone, a combination of Hemin and LY treatment induced more severe brain damage and markedly decreased the expression of pAkt. The results of the present study demonstrated that the PI3K/Akt signaling pathway, which is associated with cell survival, mediates the neuroprotective effects of Hemin‑induced Ngb following cerebral ischemia.