| 唐小卿,张盼盼,魏海军.同型半胱氨酸通过促进细胞焦亡和上调琥珀酸脱氢酶亚基A诱导神经炎症反应.[J].中南医学科学杂志.,2022,(4):469-473. |
| 同型半胱氨酸通过促进细胞焦亡和上调琥珀酸脱氢酶亚基A诱导神经炎症反应 |
| Homocysteine induces neuroinflammation by improving pyroptosis and upregulating SDHA |
| 投稿时间：2022-04-09 修订日期：2022-04-20 |
| DOI：10.15972/j.cnki.43-1509/r.2022.04.001 |
| 中文关键词: 同型半胱氨酸 细胞焦亡 琥珀酸脱氢酶亚基A 神经炎症 |
| 英文关键词:homocysteine cell pyroptosis succinate dehydrogenase subunit A neuroinflammation |
| 基金项目:国家自然科学基金项目(81971267)；湖南省自然科学基金青年项目(2020JJ5147)；湖南省教育厅科学研究一般项目(19C0650) 作者简介:唐小卿,博士,教授,博士研究生导师,研究方向为神经变性的机制及防治,E-mail为tangxq-usc@qq.com。张盼盼,硕士研究生,研究方向为神经变性的机制及防治,E-mail为zhangpp-usc@qq.com。 |
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| 中文摘要: |
| 目的探索同型半胱氨酸(Hcy)是否通过促进细胞焦亡和上调琥珀酸脱氢酶亚基A(SDHA)蛋白表达诱导神经炎症反应。 方法使用不同浓度Hcy(1.25、2.50、5.00 mmol/L)处理小鼠海马神经元细胞系HT22细胞。CCK-8检测细胞活力；免疫荧光法观察细胞形态和焦亡相关蛋白消皮素(GSDMD)与细胞膜的共定位情况；Western blotting检测细胞核苷酸结合寡聚化结构样受体蛋白3(NLRP3)、天冬氨酸蛋白水解酶-1前体(pro-Caspase-1)和Caspase-1的活性片段(cleaved-Caspase-1)、凋亡相关斑点样蛋白(ASC)、GSDMD和GSDMD的N端结构域(GSDMD-N)等焦亡相关蛋白及SDHA蛋白表达水平。酶联免疫吸附测定法检测炎症因子白细胞介素-1β(IL-1β)和白细胞介素-18(IL-18)水平。 结果Hcy可显著降低HT22细胞活力,损伤HT22细胞突触,增加GSDMD与细胞膜的共定位和细胞膜破裂程度,上调HT22细胞NLRP3、pro-Caspase-1、cleaved-Caspase-1、ASC、GSDMD和GSDMD-N等焦亡相关蛋白及SDHA蛋白表达水平,并增加IL-1β和IL-18水平。 结论Hcy可诱导神经炎症反应,其机制与其促进细胞焦亡和上调SDHA蛋白表达密切相关。 |
| 英文摘要: |
| To demonstrate whether homocysteine(Hcy) induces neuroinflammation by improving pyroptosis and upregulating the expression of succinate dehydrogenase subunit A(SDHA). MethodsHT22 cells were treated with different concentrations of homocysteine (Hcy, 1.25,2.50,5.00 mmol/L). The cell viability was tested by CCK-8. The cell morphology as well as the co-localization of gasdermin D (GSDMD) and cell membrane were observed by immunofluorescence. The expressions of pyroptosis-associated proteins, nucleotide-binding oligomerization domain-like receptorprotein 3 (NLRP3), pro-Caspase-1, cleaved-Caspase-1, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), GSDMD, and N-terminal fragment of GSDMD (GSDMD-N), as well as SDHA were detected by Western blotting. The levels of interleukin-1β (IL-1β) and interleukin-18 (IL-18) were measured by Enzyme-linked immunosorbent assay (ELISA). ResultsHcy decreased the cell viability, damaged the synapse, increased the co-localization of GSDMD and cell membrane, enhanced the rupture of cell membrane, increased the expressions of pyroptosis-related proteins, NLRP3, pro-Caspase-1, cleaved-Caspase-1, ASC, GSDMD and GSDMD-N, upregulated the expression of SDHA, elevated the levels of IL-1β and IL-18. ConclusionHcy induces neuroinflammation, which is corelated with improving pyroptosis and upregulating the expression of SDHA. |
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