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https://www.selleckchem.com/products/seclidemstat.html At P35, the learning and memory abilities were assessed in each mouse using a Morris water maze test. Dexmedetomidine significantly decreased the expression of activated caspase‑3 following sevoflurane exposure. Moreover, dexmedetomidine significantly decreased the levels of TNF‑α, IL‑1β and IL‑6 in the hippocampus. SOD activity also increased in a dose‑dependent manner in dexmedetomidine‑treated mice. MDA decreased in a dose‑dependent manner in dexmedetomidine‑treated mice. Lastly, sevoflurane‑induced learning and memory impairment was reversed by dexmedetomidine treatment. By contrast, co‑administration of yohimbine significantly attenuated the neuroprotective effects of dexmedetomidine. These findings suggested that dexmedetomidine exerted a neuroprotective effect against sevoflurane‑induced apoptosis, inflammation, oxidative stress and neurocognitive impairment, which was mediated, at least in part, by α2 adrenoceptors.Acute myocardial infarction (AMI) is a common cardiac disease. Long non‑coding RNA maternally expressed 3 (MEG3) is associated with cellular processes in numerous complicated diseases, including AMI. However, the mechanism underlying MEG3 in myocardial hypoxia is not completely understood. The present study aimed to investigate the underlying mechanism of MEG3 in myocardial hypoxia. The expression levels of hypoxia‑inducible factor 1α (HIF1α), MEG3, microRNA (miR)‑325‑3p, and transient receptor potential cation channel subfamily V member 4 (TRPV4) in hypoxia‑treated H9c2 cells were detected via reverse transcription‑quantitative PCR. The protein expression levels of HIF1α, Bcl‑2, Bax, cleaved caspase‑3 and TRPV4 were detected via western blotting. Cell viability and apoptosis were assessed by performing an MTT assay and flow cytometry, respectively. Lactate dehydrogenase (LDH) release was monitored by conducting an LDH determination assay. The dual‑luciferase reporter assay was performed to ve

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