Molecular biology reports
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Molecular biology reports · Oct 2020
Dexmedetomidine alleviates sevoflurane-induced neurotoxicity via mitophagy signaling.
Dexmedetomidine, a class of α2-adrenergic agonist, was reported to exert a neuroprotective effect on sevoflurane-induced neurotoxicity. However, the specific mechanisms have not been fully clarified yet. The aim of our study is to uncover the role of dexmedetomidine in sevoflurane-induced neurotoxicity. The rats pretreated with dexmedetomidine and/or Rapamycin 3-Methyladenine were housed in a box containing 30% O2, 68% N2 and 2% sevoflurane for 4 h for anesthesia. 24 h after drug injection, Morris water maze test was used to evaluate rats' learning and memory ability. ⋯ Dexmedetomidine alleviated sevoflurane-induced nerve injury and the impairment of learning and memory abilities. Additionally, dexmedetomidine inhibited sevoflurane-induced cell apoptosis in hippocampus. In mechanism, dexmedetomidine activated mitophagy to mitigate neurotoxicity by enhancing LC3II/LC3I ratio, HSP60, Beclin-1, CypD, VDAC1 and Tom20 protein levels in hippocampus. Dexmedetomidine alleviates sevoflurane-induced neurotoxicity via mitophagy signaling, offering a potential strategy for sevoflurane-induced neurotoxicity treatment.
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Molecular biology reports · Oct 2020
Clinical TrialInvestigation of telomere related gene mutations in idiopathic pulmonary fibrosis.
Idiopathic Pulmonary Fibrosis (IPF) is the most common type of Idiopathic Interstitial Pneumonias (IIP). The aim of this study is to determine the mutation of variants in four telomere-related genes and to determine the possible relationship between these mutations and telomere shortening in order to contribute to the understanding of the pathophysiology of IPF. For this study, 34 individuals with IPF, 32 individuals with non-IPF ILD (Interstitial Lung Disease), and 31 healthy controls between the ages of 40 and 85 were included. ⋯ However, in terms of the allele distribution for two genes, statistically significant difference was found in IPF and non-IPF ILD patients (TERT; p = 0.002 and TERC; p = 0.001). According to the telomere length measurement, the telomeres of the patients were shorter than of the control group (p = 0.0001). In compliance with the results of our analysis, it is thought that genes that have allelic significance from the point of gene mutations as well as telomere shortening may be risk factors for the disease.