Xueyan Hu1, Xiaodong Hu1, Guirong Huang1. 1. Department of Anesthesiology, Yishui Central Hospital, Linyi, People's Republic of China.
Abstract
OBJECTIVE: The purpose of this study is to uncover the effects of long chain noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on sevoflurane-induced neurotoxicity in developing rats. METHODS: Sevoflurane neurotoxicity model was established by sevoflurane treatment in 7-day-old Sprague-Dawley rats. The rats were treated with Sevo or MALAT1 small interfering RNA to detect the MALAT1 expression, pathological change, ultrastructure, neuronal apoptosis, expression of apoptosis-related proteins, expression of neurotrophic factors BDNF and NGF, spatial learning and memory function change, as well as neuron cell density of hippocampal tissues. RESULTS: MALAT1 was highly expressed in hippocampus tissues of rats. Downregulation of MALAT1 alleviated the pathological change, improved the ultrastructure, inhibited apoptosis of neuronal cells, declined caspase 3 and Bax while elevated Bcl-2, BDNF and NGF, improved capability of spatial learning and memory, and increased density of hippocampal neurons in hippocampal tissues of sevoflurane-induced rats. CONCLUSION: Suppression of MALAT1 can reduce the apoptosis of hippocampal neurons induced by sevoflurane anesthesia, improve the capability of spatial learning, and memory function and alleviate the loss of hippocampal nerve cells in developing rats. To a certain extent, it plays the role of protecting brain nerve cells.
OBJECTIVE: The purpose of this study is to uncover the effects of long chain noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on sevoflurane-induced neurotoxicity in developing rats. METHODS:Sevofluraneneurotoxicity model was established by sevoflurane treatment in 7-day-old Sprague-Dawley rats. The rats were treated with Sevo or MALAT1 small interfering RNA to detect the MALAT1 expression, pathological change, ultrastructure, neuronal apoptosis, expression of apoptosis-related proteins, expression of neurotrophic factors BDNF and NGF, spatial learning and memory function change, as well as neuron cell density of hippocampal tissues. RESULTS: MALAT1 was highly expressed in hippocampus tissues of rats. Downregulation of MALAT1 alleviated the pathological change, improved the ultrastructure, inhibited apoptosis of neuronal cells, declined caspase 3 and Bax while elevated Bcl-2, BDNF and NGF, improved capability of spatial learning and memory, and increased density of hippocampal neurons in hippocampal tissues of sevoflurane-induced rats. CONCLUSION: Suppression of MALAT1 can reduce the apoptosis of hippocampal neurons induced by sevoflurane anesthesia, improve the capability of spatial learning, and memory function and alleviate the loss of hippocampal nerve cells in developing rats. To a certain extent, it plays the role of protecting brain nerve cells.