| 张慧宇,白振军,李 亮,张金锋,解佳伟,邓 亮,孟 燕,郭敏芳.雷公藤甲素通过抑制 NogoA/ RhoA/ ROCK 信号通路 减轻氧糖剥夺 / 复糖复氧所致的 SH-SY5Y 细胞损伤[J].中国比较医学杂志,2023,33(1):9~15. |
| 雷公藤甲素通过抑制 NogoA/ RhoA/ ROCK 信号通路 减轻氧糖剥夺 / 复糖复氧所致的 SH-SY5Y 细胞损伤 |
| Triptolide attenuates oxygen glucose deprivation / reoxygenation-induced SH-SY5Y cell injury by inhibiting the NogoA / RhoA / ROCK signaling pathway |
| 投稿时间：2022-05-19 |
| DOI：10. 3969 / j.issn.1671-7856. 2023. 01. 002 |
| 中文关键词: 雷公藤甲素 氧糖剥夺/ 复糖复氧 神经突生长抑制因子 A Rho 激酶 突触可塑性 |
| 英文关键词:triptolide oxygen-glucose deprivation / reoxygenation neurite outgrowth inhibitor A Rho kinase synaptic plasticity |
| 基金项目: |
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| Author Name | Affiliation | | ZHANG Huiyu | College of Traditional Chinese Medicine Health Service, Shanxi Datong University, Datong 037009, China | | BAI Zhenjun | College of Traditional Chinese Medicine Health Service, Shanxi Datong University, Datong 037009, China | | LI Liang | College of Traditional Chinese Medicine Health Service, Shanxi Datong University, Datong 037009, China | | ZHANG Jinfeng | College of Traditional Chinese Medicine Health Service, Shanxi Datong University, Datong 037009, China | | XIE Jiawei | College of Traditional Chinese Medicine Health Service, Shanxi Datong University, Datong 037009, China | | DENG Liang | College of Traditional Chinese Medicine Health Service, Shanxi Datong University, Datong 037009, China | | MENG Yan | College of Traditional Chinese Medicine Health Service, Shanxi Datong University, Datong 037009, China | | GUO Minfang | Medical College, Shanxi Datong University, Datong 037009 |
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| 中文摘要: |
| 目的 基于 Nogo-A/ RhoA/ ROCK 信号通路探讨雷公藤甲素减轻氧糖剥夺/ 复糖复氧(OGD/ R)诱导的 SH-SY5Y 细胞损伤的机制。 方法 CCK8 法检测不同浓度雷公藤甲素对正常 SH-SY5Y 细胞活性的影响以筛选最佳的药物作用浓度;然后将 SH-SY5Y 细胞分为 4 组:正常对照组、模型组、雷公藤甲素(1 nmol / L)干预组、Rho 激酶抑制剂法舒地尔(15 μg / mL)干预组。 CCK8 法检测 SH-SY5Y 细胞活性;JC-1 试剂盒评估线粒体膜电位;免疫荧 光染色检测 NogoA、ROCK2 和 GAP43 的表达;Western blot 法检测 GAP43、PSD95、NogoA、NgR、RhoA 和 ROCK2 的表达。 结果 CCK8 结果显示,雷公藤甲素的最适作用浓度为 1 nmol / L。 与正常对照组比较,模型组细胞活性降低(P<0. 001);线粒体膜电位下调(P<0. 001);GAP43 和 PSD95 表达降低(P<0. 001);同时 NogoA、NgR、RhoA 和 ROCK2 表达增加(P<0. 001);雷公藤甲素干预和法舒地尔干预均可以改善 OGD/ R 诱导的细胞损伤,使细胞活性增加(P< 0. 001),线粒体膜电位上升(P< 0. 001);上调 GAP43 和 PSD95 表达( P< 0. 05);同时下调 NogoA、NgR、RhoA 和 ROCK2 的表达(P<0. 001)。 结论 雷公藤甲素可以通过抑制 NogoA/ RhoA/ ROCK 信号通路减轻 OGD/ R 诱导的 SH-SY5Y 细胞损伤。 |
| 英文摘要: |
| Objective To explore the mechanism of triptolide reducing oxygen glucose deprivation / reoxygenation (OGD/ R)-induced SH-SY5Y cell injury via the NogoA/ RhoA/ ROCK signaling pathway. Methods The effect of various triptolide concentrations on SH-SY5Y cell proliferation was assessed by CCK8 assays to select the optimal concentration. Cells were divided into normal control, model, triptolide (1 nmol / L) treatment and fasudil (15 μg / mL) treatment groups. Cell proliferation was assessed by CCK8 assays. A JC-1 assay was used to measure the mitochondrial membrane potential. NogoA, ROCK2 and GAP43 expression was detected by immunofluorescence staining. GAP43, PSD95, NogoA, NgR, RhoA and ROCK2 expression was detected by Western blot. Results CCK8 assays showed that the optimal concentration of triptolide was 1 nmol / L. Cell proliferation and the mitochondrial membrane potential of the model group were significantly lower than those of the control group ( P< 0. 001). Compared with the control group, GAP43 and PSD95 expression was decreased and NogoA, NgR, RhoA and ROCK2 expression was increased in the model group (P<0. 001). Both triptolide and fasudil increased cell proliferation (P<0. 001) the and mitochondrial membrane potential (P<0. 001), upregulated GAP43 and PSD95 expression (P<0. 05), and downregulated NogoA, NgR, RhoA and ROCK2 expression (P<0. 001). Conclusions Triptolide may alleviate OGD/ R-induced SH-SY5Y cell injury by inhibiting the NogoA/ RhoA/ ROCK signaling pathway. |
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