SNAP25 protects primary cortical neurons from hypoxic‐ischemic injury associated with CREB signal
Background Hypoxic‐ischemic encephalopathy (HIE) could induce exacerbated changes and unpredictable effects in brain cells, and the mechanism remains unclear. Methods HIE model was established in neonatal rats, Zea‐Longa score and TTC staining were used to observe the neurobehavior and brain infarct...
| Váldodahkkit: | , , , , , , , , , |
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| Materiálatiipa: | Artihkal |
| Giella: | English |
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Wiley-VCH
2021-03-01
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| Ráidu: | Ibrain |
| Fáttát: | |
| Liŋkkat: | https://doi.org/10.1002/j.2769-2795.2021.tb00058.x |
| _version_ | 1828156662356115456 |
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| author | Yuan Jin Chao Zhang Xu Fang Chang‐Le Fang Jie Chen Ruo‐Lan Du Qiao Hu Liang Dong Zhao‐Qiong Zhu Ting‐Hua Wang |
| author_facet | Yuan Jin Chao Zhang Xu Fang Chang‐Le Fang Jie Chen Ruo‐Lan Du Qiao Hu Liang Dong Zhao‐Qiong Zhu Ting‐Hua Wang |
| author_sort | Yuan Jin |
| collection | DOAJ |
| description | Background Hypoxic‐ischemic encephalopathy (HIE) could induce exacerbated changes and unpredictable effects in brain cells, and the mechanism remains unclear. Methods HIE model was established in neonatal rats, Zea‐Longa score and TTC staining were used to observe the neurobehavior and brain infarct volume in rats subjected to cerebral hypoxia‐ischemia (HI). Primary cortical neurons were then cultured in vitro to establish an oxygen and glucose deprivation model. To determine the role of synaptosomal‐associated protein‐25 (SNAP25) in HIE, PC12 cells were cultured and effective siRNA fragments were screened, and SNAP25 was transfected into primary neurons. Then, quantitative real‐time polymerase chain reaction was used to detect the mRNA expression level and immunofluorescence staining was used to observe the morphological changes of neurons before and after the injury. Finally, the abundance values of SNAP25 and its associated genes were filtered using the NCBI and GeneMANIA, respectively. Results HI leads to a decrease in neuronal number and an increase in SNAP25 expression. Whereas, the interference of SNAP25 caused marked decrease in neuronal number and the length of neurite. Moreover, the expression levels of CREB and SYP were significantly decreased after interference of SNAP25. Conclusion SNAP25 exhibited several neuroprotective effects to neuronal protection in neonatal cerebral HI by regulating CREB and SYP. |
| first_indexed | 2024-04-11T23:14:52Z |
| format | Article |
| id | doaj.art-00e2023264ae4d1d84d97768d9a7cb15 |
| institution | Directory Open Access Journal |
| issn | 2769-2795 |
| language | English |
| last_indexed | 2024-04-11T23:14:52Z |
| publishDate | 2021-03-01 |
| publisher | Wiley-VCH |
| record_format | Article |
| series | Ibrain |
| spelling | doaj.art-00e2023264ae4d1d84d97768d9a7cb152022-12-22T03:57:38ZengWiley-VCHIbrain2769-27952021-03-017111110.1002/j.2769-2795.2021.tb00058.xSNAP25 protects primary cortical neurons from hypoxic‐ischemic injury associated with CREB signalYuan Jin0Chao Zhang1Xu Fang2Chang‐Le Fang3Jie Chen4Ruo‐Lan Du5Qiao Hu6Liang Dong7Zhao‐Qiong Zhu8Ting‐Hua Wang9Institute of Neuroscience, Kunming Medical UniveristyKunmingYunnanChinaDepartment of AnesthesiologyGuizhou Key Laboratory of Anesthesia and Organ Protection, Affiliated Hospital of Zunyi Medical UniversityZunyiGuizhouChinaDepartment of AnesthesiologyGuizhou Key Laboratory of Anesthesia and Organ Protection, Affiliated Hospital of Zunyi Medical UniversityZunyiGuizhouChinaNational Traditional Chinese Medicine Clinical Research Base and Western Medicine Translational Medicine Research CenterDepartment of AnesthesiologyDepartment of Cardiovascular DiseaseAffiliated Traditional Chinese Medicine Hospital, Southwest Medical UniversityLuzhouSichuanChinaNational Traditional Chinese Medicine Clinical Research Base and Western Medicine Translational Medicine Research CenterDepartment of AnesthesiologyDepartment of Cardiovascular DiseaseAffiliated Traditional Chinese Medicine Hospital, Southwest Medical UniversityLuzhouSichuanChinaInstitute of Neuroscience, Kunming Medical UniveristyKunmingYunnanChinaInstitute of Neuroscience, Kunming Medical UniveristyKunmingYunnanChinaDepartment of AnesthesiologyGuizhou Key Laboratory of Anesthesia and Organ Protection, Affiliated Hospital of Zunyi Medical UniversityZunyiGuizhouChinaDepartment of AnesthesiologyGuizhou Key Laboratory of Anesthesia and Organ Protection, Affiliated Hospital of Zunyi Medical UniversityZunyiGuizhouChinaInstitute of Neuroscience, Kunming Medical UniveristyKunmingYunnanChinaBackground Hypoxic‐ischemic encephalopathy (HIE) could induce exacerbated changes and unpredictable effects in brain cells, and the mechanism remains unclear. Methods HIE model was established in neonatal rats, Zea‐Longa score and TTC staining were used to observe the neurobehavior and brain infarct volume in rats subjected to cerebral hypoxia‐ischemia (HI). Primary cortical neurons were then cultured in vitro to establish an oxygen and glucose deprivation model. To determine the role of synaptosomal‐associated protein‐25 (SNAP25) in HIE, PC12 cells were cultured and effective siRNA fragments were screened, and SNAP25 was transfected into primary neurons. Then, quantitative real‐time polymerase chain reaction was used to detect the mRNA expression level and immunofluorescence staining was used to observe the morphological changes of neurons before and after the injury. Finally, the abundance values of SNAP25 and its associated genes were filtered using the NCBI and GeneMANIA, respectively. Results HI leads to a decrease in neuronal number and an increase in SNAP25 expression. Whereas, the interference of SNAP25 caused marked decrease in neuronal number and the length of neurite. Moreover, the expression levels of CREB and SYP were significantly decreased after interference of SNAP25. Conclusion SNAP25 exhibited several neuroprotective effects to neuronal protection in neonatal cerebral HI by regulating CREB and SYP.https://doi.org/10.1002/j.2769-2795.2021.tb00058.xNeonatal hypoxia and ischemiaSNAP25Oxygen and glucose deprivation |
| spellingShingle | Yuan Jin Chao Zhang Xu Fang Chang‐Le Fang Jie Chen Ruo‐Lan Du Qiao Hu Liang Dong Zhao‐Qiong Zhu Ting‐Hua Wang SNAP25 protects primary cortical neurons from hypoxic‐ischemic injury associated with CREB signal Ibrain Neonatal hypoxia and ischemia SNAP25 Oxygen and glucose deprivation |
| title | SNAP25 protects primary cortical neurons from hypoxic‐ischemic injury associated with CREB signal |
| title_full | SNAP25 protects primary cortical neurons from hypoxic‐ischemic injury associated with CREB signal |
| title_fullStr | SNAP25 protects primary cortical neurons from hypoxic‐ischemic injury associated with CREB signal |
| title_full_unstemmed | SNAP25 protects primary cortical neurons from hypoxic‐ischemic injury associated with CREB signal |
| title_short | SNAP25 protects primary cortical neurons from hypoxic‐ischemic injury associated with CREB signal |
| title_sort | snap25 protects primary cortical neurons from hypoxic ischemic injury associated with creb signal |
| topic | Neonatal hypoxia and ischemia SNAP25 Oxygen and glucose deprivation |
| url | https://doi.org/10.1002/j.2769-2795.2021.tb00058.x |
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