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>Overexpression of IncRNA Gml5621 alleviates apoptosis and inflammation response resulting from sevoflurane treatment through inhibiting miR-133a/Sox4
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Overexpression of IncRNA Gml5621 alleviates apoptosis and inflammation response resulting from sevoflurane treatment through inhibiting miR-133a/Sox4
Sevoflurane is the most widely used anesthetic administered by inhalation. Exposure to sevoflurane can elicit learning deficits and abnormal cognitive disorder. In this study, we investigated the function of long noncoding RNA (IncRNA) Gml5621. Primary hippocampal neuron cells were used to analyze the function of IncRNA Gml5621 in vitro. The tunel, inflammation markers, and cell survival rates were detected to evaluate the function of IncRNA Gml5621. Dual-luciferase reporter assay was used to identify the interaction between microRNA 133a and Gml5621. We found that IncRNA Gml5621 located in the cytoplasm. The expression of IncRNA Gml5621 was decreased with the development of sevoflurane exposure. Over-expression of IncRNA Gml5621 significantly reduced the apoptosis and cell survival rates. The inflammation response was also attenuated in IncRNA Gml5621 overexpressed group. The dual-luciferase assay revealed that miR-133a was the direct target of IncRNA Gml5621. In addition, we also found that Sox4 was a downstream target of miR-133a and IncRNA Gml5621 exerted its biological functions by regulating the expression of Sox4. In summary, our findings revealed that IncRNA Gml5621 ameliorated the sevoflurane-induced neurotoxicity and the important role of Gml5621/miR-133a/Sox4 axis in cognitive disorder.
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