Drug Des Dev Ther
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Premedication is the most common way to minimize distress in children entering the operating room and to facilitate the smooth induction of anesthesia and is accomplished using various sedative drugs before the children are being transferred to the operating room. The aim of this study was to compare the effect of oral dexmedetomidine (DEX) and oral midazolam (MID) on preoperative cooperation and emergence delirium (ED) among children who underwent dental procedures at our hospital between 2016 and 2017. ⋯ Oral DEX provided satisfactory sedation levels, ease of parental separation, and mask acceptance in children in a manner similar to MID. Moreover, children premedicated with DEX experienced lesser ED than those premedicated with MID.
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Recent evidence has shown the involvement of inflammation in the development of diabetic peripheral neuropathy (DPN). MicroRNA-146a (miR-146a) is closely involved in the inflammatory response. However, the role of miR-146a in the inflammatory reaction in DPN has not been clarified. This study was designed to explore the role of miR-146a in the regulation of inflammatory responses in DPN. ⋯ miR-146a is involved in the pathogenesis of DPN, and its expression level is closely related to the inflammatory responses that aggravate sciatic nerve injuries.
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The effect of sevoflurane on the nervous system is controversial. As an adjuvant anesthetic, dexmedetomidine has a protective role in various nerve-injury diseases. We investigated the effect of dexmedetomidine on injury to the developing brain induced by sevoflurane anesthesia, and if autophagy and mitochondrial damage are involved in the neuroprotective effects of dexmedetomidine. ⋯ Sevoflurane exposure during the third trimester caused neurological injury to rat pups. Autophagy and abnormalities in mitochondrial dynamics were involved in this neurotoxic process and were antagonized by dexmedetomidine.
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Sevoflurane post-conditioning exerts nerve-protective effects through inhibiting caspase-dependent neuronal apoptosis after a traumatic brain injury (TBI). Autophagy that is induced by the endoplasmic reticulum stress plays an important role in the secondary neurological dysfunction after a TBI. However, the relationship between autophagy and caspase-dependent apoptosis as well as the underlying nerve protection mechanism that occurs with sevoflurane post-conditioning following a TBI remains unclear. ⋯ Neuronal apoptosis and the activation of autophagy were involved in the secondary neurological injury following a TBI. Sevoflurane post-conditioning weakened the TBI-induced neuronal apoptosis by regulating autophagy via PI3K/AKT signaling.
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The neuroprotective effects of Baicalin have been confirmed in several central nervous system (CNS) diseases. However, its possible effect on traumatic brain injury (TBI) model is still not clear. The present study is aimed to investigate the role and the underling mechanisms of 7-D-glucuronic acid-5,6-dihydroxyflavone (Baicalin) on TBI model. ⋯ This study demonstrates that Baicalin provides a neuroprotective effect in TBI mice model via activating the Akt/Nrf2 pathway.