Yanqiu Ai
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Yanqiu Ai has a total of 6 co-authors. Here are the top co-authors by number of shared publications:
Yanling Zhao
Department of Anesthesiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China
3 shared publications- Chunlan Liu
Department of Epidemiology, School of Public Health, Nanjing Medical University, Nanjing 211166, China
1 shared publication - Long He
State Key Laboratory for Quality and Safety of Agro-Products, Institute of Plant Virology, Ningbo University, Ningbo 315211, China
1 shared publication - Qi Zhang
Basic Medicine Department, Hangzhou Medical College, Hangzhou 310053, China
1 shared publication - Qinjun Chu
Department of Anesthesiology and Perioperative Medicine, Zhengzhou Central Hospital Affiliated to Zhengzhou University
1 shared publication - Wei Zhang
Department of Colorectal Surgery, Changhai Hospital, Naval Medical University, Shanghai, China
1 shared publication
Latest Publications
- 1 July 2020
- Published by Elsevier in Life Sciences
- Vol. 253, 117769
Corrigendum to “Knockdown of lncRNA MALAT1 promotes bupivacaine-induced neurotoxicity via the miR-101-3p/PDCD4 axis” [Life Sci. 232 (2019) 116606]
- 1 July 2020
- Published by Elsevier in Life Sciences
- Vol. 253, 117769
Corrigendum to “Knockdown of lncRNA MALAT1 promotes bupivacaine-induced neurotoxicity via the miR-101-3p/PDCD4 axis” [Life Sci. 232 (2019) 116606]
- 1 September 2019
- Published by Elsevier in Life Sciences
- Vol. 232, 116606
Knockdown of lncRNA MALAT1 alleviates bupivacaine-induced neurotoxicity via the miR-101-3p/PDCD4 axis
- 1 September 2019
- Published by Elsevier in Life Sciences
- Vol. 232, 116606
Knockdown of lncRNA MALAT1 alleviates bupivacaine-induced neurotoxicity via the miR-101-3p/PDCD4 axis
- 2 July 2019
- Published by Wiley in Journal of Cellular Physiology
- Vol. 235 (2) , 957-965
Overexpression of lncRNA Gm15621 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 (lncRNA) Gm15621. Primary hippocampal neuron cells were used to analyze the function of lncRNA Gm15621 in vitro. The tunel, inflammation markers, and cell survival rates were detected to evaluate the function of lncRNA Gm15621. Dual‐luciferase reporter assay was used to identify the interaction between microRNA 133a and Gm15621. We found that lncRNA Gm15621 located in the cytoplasm. The expression of lncRNA Gm15621 was decreased with the development of sevoflurane exposure. Overexpression of lncRNA Gm15621 significantly reduced the apoptosis and cell survival rates. The inflammation response was also attenuated in lncRNA Gm15621 overexpressed group. The dual‐luciferase assay revealed that miR‐133a was the direct target of lncRNA Gm15621. In addition, we also found that Sox4 was a downstream target of miR‐133a and lncRNA Gm15621 exerted its biological functions by regulating the expression of Sox4. In summary, our findings revealed that lncRNA Gm15621 ameliorated the sevoflurane‐induced neurotoxicity and the important role of Gm15621/miR‐133a/Sox4 axis in cognitive disorder.
- 2 July 2019
- Published by Wiley in Journal of Cellular Physiology
- Vol. 235 (2) , 957-965
Overexpression of lncRNA Gm15621 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 (lncRNA) Gm15621. Primary hippocampal neuron cells were used to analyze the function of lncRNA Gm15621 in vitro. The tunel, inflammation markers, and cell survival rates were detected to evaluate the function of lncRNA Gm15621. Dual‐luciferase reporter assay was used to identify the interaction between microRNA 133a and Gm15621. We found that lncRNA Gm15621 located in the cytoplasm. The expression of lncRNA Gm15621 was decreased with the development of sevoflurane exposure. Overexpression of lncRNA Gm15621 significantly reduced the apoptosis and cell survival rates. The inflammation response was also attenuated in lncRNA Gm15621 overexpressed group. The dual‐luciferase assay revealed that miR‐133a was the direct target of lncRNA Gm15621. In addition, we also found that Sox4 was a downstream target of miR‐133a and lncRNA Gm15621 exerted its biological functions by regulating the expression of Sox4. In summary, our findings revealed that lncRNA Gm15621 ameliorated the sevoflurane‐induced neurotoxicity and the important role of Gm15621/miR‐133a/Sox4 axis in cognitive disorder.
- 1 July 2013
- Published by Elsevier in Journal of Surgical Research
- Vol. 183 (1) , 330-336
Hydrogen sulfide attenuates surgical trauma-induced inflammatory response and cognitive deficits in mice
- 1 July 2013
- Published by Elsevier in Journal of Surgical Research
- Vol. 183 (1) , 330-336
Hydrogen sulfide attenuates surgical trauma-induced inflammatory response and cognitive deficits in mice