Molecular medicine reports
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General anesthesia is commonly used in the surgical arena, but little is known regarding its influence at the genomic and molecular levels. MicroRNAs (miRNAs) belong to a new class of non-coding RNA molecules which influence cell biology. In the present study, it was hypothesized that miRNAs alter gene expression levels under general anesthesia. ⋯ By contrast, following propofol anesthesia, the levels of 11 miRNAs were significantly reduced but no miRNAs exhibited significantly elevated levels. One miRNA was common between the two anesthesia groups, whereas 14 miRNAs were significantly differentially expressed. In conclusion, sevoflurane and propofol exerted different effects on miRNA expression in the rat hippocampus.
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Previous studies have demonstrated that progesterone has neuroprotective effects in the central nervous system (CNS) following traumatic brain injury (TBI). Numerous cellular mechanisms have been reported to be important in the neuroprotective effects of progesterone, including the reduction of edema, inflammation and apoptosis, and the inhibition of oxidative stress. However, the effect of progesterone on neuronal protection following TBI remains unclear. ⋯ TBI rats significantly increased the expression of Nogo-A, GFAP, and GAP-43 at 1, 3, 7 and 14 days post-injury. Progesterone significantly decreased the expression of Nogo-A and GFAP, and upregulated the GAP-43 protein. Our findings suggested that progesterone promotes neuroprotection following TBI by inhibiting the expression of Nogo-A and GFAP, and increasing GAP-43 expression.
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Obesity is associated with increased infarct volumes and adverse outcomes following ischemic stroke. However, its effect on anesthetic postconditioning‑induced neuroprotection has not been investigated. The present study examined the effect of sevoflurane postconditioning on focal ischemic brain injury in diet‑induced obesity. ⋯ Pretreatment with 5‑HD inhibited sevoflurane‑induced neuroprotection in the LF‑fed rats, whereas it had no effect in the HF‑fed rats. Molecular studies demonstrated that the expression of Kir6.2, a significant mitoKATP channel component, was reduced in the brains of the HF‑fed rats compared with the LF‑fed rats. The results of this study indicate that diet‑induced obesity eliminates the ability of anesthetic sevoflurane postconditioning to protect the brain against cerebral ischemic neuronal injury, most likely due to an impaired brain mitoKATP channel.
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Dexmedetomidine, a specific selective α2-adrenergic agonist, does not only have the characteristics of being a sedative and analgesic, but also exhibits a protective role in brain ischemia-reperfusion injury and inhibits the inflammation in animals with sepsis. The objective of the present study was to investigate whether dexmedetomidine is capable of attenuating rat pulmonary damage induced by ischemia-reperfusion injury, which is a type of acute sterile lung injury. Sprague-Dawley rats were randomly assigned into six groups: The sham-operated (sham) group, the lung ischemia-reperfusion (I/R) group, intravenous injection of dexmedetomidine 2.5 µg/kg/h (Dex2.5) or 5 µg/kg/h (Dex5) for 1 h prior to ischemia, combination of α2-adrenergic antagonist yohimbine prior to dexmedetomidine pre-treatment (Dex+Yoh) and pre-administration of yohimbine alone (Yoh) prior to ischemia. ⋯ The protective effects of dexmedetomidine on the lung were not completely reversed by the α2-adrenergic antagonist, yohimbine. Pre-treatment with dexmedetomidine is capable of reducing pulmonary damage and inhibiting sterile inflammation induced by lung I/R injury. TLR4/MyD88/mitogen-activated protein kinase (MAPK) signaling is involved in the protective mechanism of dexmedetomidine through α2-adrenoceptor independence.
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The aim of the current study was to investigate the effect of chronic dexamethasone (Dex) administration on rat diaphragm function and sensitivity to rocuronium and muscle‑fiber transformation. Adult male Sprague‑Dawley rats were randomized to receive a daily intraperitoneal injection of Dex to evaluate whether alterations in diaphragm function and susceptibility to rocuronium would be induced. In addition, diaphragm contractile properties, histopathology and isometric twitch tensions of nerve‑hemidiaphragm preparations were evaluated. ⋯ Dex treatment led to desensitization of the rat diaphragm to rocuronium, as demonstrated by a shift of the rocuronium concentration‑twitch tension curves to the right. Histochemical analysis of adenosine triphosphatase revealed that the distribution and cross‑sectional area of type II fibers were decreased in rats exposed to Dex. The present study indicates that chronic Dex treatment induced alterations in muscle function and that susceptibility to rocuronium is associated with muscle fiber‑type transformation, which may aid in directing future administration of muscle relaxants.