| 引用本文: | 卢仁睿,张莉,王慧慧,李孟,郑晓珂,冯卫生.桃叶珊瑚苷对谷氨酸诱导的兴奋性神经毒性的抑制作用研究[J].中国现代应用药学,2022,39(24):3197-3203. |
| LU Renrui,ZHANG Li,WANG Huihui,LI Meng,ZHENG Xiaoke,FENG Weisheng.Study on the Inhibitory Effect of Aucubin on Glutamate-Induced Excitatory Neurotoxicity[J].Chin J Mod Appl Pharm(中国现代应用药学),2022,39(24):3197-3203. |
|
| |
|
|
| 本文已被：浏览 831次 下载 404次 |
码上扫一扫！ |
|
|
| 桃叶珊瑚苷对谷氨酸诱导的兴奋性神经毒性的抑制作用研究 |
|
卢仁睿1, 张莉1, 王慧慧1, 李孟1, 郑晓珂1,2, 冯卫生1,2
|
|
1.河南中医药大学药学院, 郑州 450046;2.河南省中药开发工程技术研究中心, 郑州 450046
|
|
| 摘要: |
| 目的 研究桃叶珊瑚苷对谷氨酸诱导的兴奋性神经毒性的抑制作用。方法 采用20 mmol·L-1谷氨酸诱导PC-12细胞损伤建立神经毒性模型,加入1,5,10,20,40 μmol·L-1的桃叶珊瑚苷处理24 h后,通过MTT法检测细胞活力,用流式细胞术检测细胞内Ca2+和活性氧(reactive oxygen species,ROS)水平,采用In Cell Western检测谷氨酸受体N-甲基-D-天冬氨酸受体(N-methyl-D-aspartic acid receptor,NMDA)亚基NMDAR1的水平,采用ELISA试剂盒检测细胞上清中超氧化物歧化酶(superoxide dismutase,SOD)、丙二醛(malondialdehyde,MDA)、乳酸脱氢酶(lactate dehydrogenase,LDH)水平。结果 谷氨酸20 mmol·L-1作用24 h可使体外培养的PC-12细胞活力明显下降(P<0.01),细胞内Ca2+、NMDAR1蛋白水平和ROS、MDA、LDH水平明显增加(P<0.01),SOD水平明显降低。10 μmol·L-1的桃叶珊瑚苷可以明显提高谷氨酸诱导后PC-12细胞的细胞活力(P<0.01),降低细胞内Ca2+、NMDAR1蛋白水平和ROS、LDH水平(P<0.01),升高细胞内SOD水平(P<0.01)。结论 桃叶珊瑚苷可能通过抑制NMDAR1的表达,从而降低细胞内Ca2+的堆积,并抑制氧化应激水平来改善谷氨酸诱导的PC-12细胞损伤,抑制谷氨酸诱导的兴奋性神经毒性。 |
| 关键词: 桃叶珊瑚苷 N-甲基-D-天冬氨酸受体亚基 细胞内Ca2+水平 谷氨酸 PC-12 |
| DOI：10.13748/j.cnki.issn1007-7693.2022.24.002 |
| 分类号:R285.5 |
| 基金项目:国家重点研发计划中医药现代化研究重点专项(2017YFC1702800)；河南省重大科技专项项目(171100310500)；河南省高层次人才特殊支持计划“中原千人计划”-中原领军人才(ZYQR201810080)；河南省教育厅河南省科技攻关项目(212102311106)；河南省中医药科学研究专项课题(20-21ZY2151) |
|
| Study on the Inhibitory Effect of Aucubin on Glutamate-Induced Excitatory Neurotoxicity |
|
LU Renrui1, ZHANG Li1, WANG Huihui1, LI Meng1, ZHENG Xiaoke1,2, FENG Weisheng1,2
|
|
1.School of Pharmacy, Henan University of Chinese Medicine, Zhengzhou 450046, China;2.Henan Engineering Technology Research Center for Chinese Medicine Development, Zhengzhou 450046, China
|
| Abstract: |
| OBJECTIVE To investigate the inhibitory effect of aucubin on glutamate-induced excitatory neurotoxicity. METHODS A neurotoxicity model was established using 20 mmol·L-1glutamate to induce damage in PC-12 cells. After treatment with 1, 5, 10, 20 and 40 μmol·L-1 aucubin for 24 h, cell viability was measured by MTT, intracellular Ca2+ and reactive oxygen species(ROS) levels were measured by flow cytometry, the level of glutamate receptor N-methyl-D-aspartic acid receptor(NMDAR1) were measured by In Cell Western. And superoxide dismutase(SOD), malondialdehyde(MDA), and lactate dehydrogenase(LDH) levels in cell supernatants were measured by using ELISA kits. RESULTS After treated with 20 mmol·L-1glutamate for 24 h, the viability of PC-12 cells was significantly reduced(P<0.01), the levels of intracellular Ca2+, NMDAR1 ROS, MOA, LDH were significantly increased (P<0.01), the level of SOD was significantly reduced. 10 μmol·L-1 aucubin could significantly increase the cell viability of PC-12 cells injured by glutamate(P<0.01), it could reduce the levels of intracellular Ca2+, NMDAR1, ROS and LDH(P<0.01), and elevate intracellular SOD level(P<0.01). CONCLUSION Aucubin may ameliorate glutamate-induced damage in PC-12 cells by inhibiting NMDAR1 expression, thereby reducing the accumulation of intracellular Ca2+, and inhibiting oxidative stress levels to suppress glutamate-induced excitatory neurotoxicity. |
| Key words: aucucbin N-methyl-D-aspartic acid receptor subunit intracellular Ca2+ level glutamate PC-12 |
|
|
|
|
