| 吴基林,李慧娴,李义红,等.瞬时感受器电位离子通道香草素受体亚家族 Ⅳ在帕金森病细胞模型中介导 PC12细胞炎症反应的机制[J].安徽医药,2024,28(11):2165-2168. |
| 瞬时感受器电位离子通道香草素受体亚家族 Ⅳ在帕金森病细胞模型中介导 PC12细胞炎症反应的机制 |
| Mechanism of transient receptor potential vanillin receptor subfamily Ⅳ mediating inflammation of PC12 cells in Parkinson's disease cell model |
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| DOI：10.3969/j.issn.1009-6469.2024.11.010 |
| 中文关键词: TRPV阳离子通道 香草素受体亚家族 Ⅳ 帕金森病 炎症反应 细胞模型 显升高， |
| 英文关键词: TRPV cation channels Transient receptor potential vanillin receptor subfamily Ⅳ Parkinson's disease Inflammation Cell model |
| 基金项目:国家自然科学基金项目( 82260236)；云南省科学技术厅 -昆明医科大学应用基础研究联合专项( 202301AY070001-074)；云南省中青年“学术和技术带头人”后备人才项目( 202405AC350087) |
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| 中文摘要: |
| 目的探讨瞬时感受器电位离子通道香草素受体亚家族 Ⅳ(TRPV4)在帕金森病( PD)细胞模型中介导 PC12细胞炎症反应的机制。方法 2023年 6―8月，用 1-甲基 -4-苯基吡啶离子( MPP+)建立 PD细胞模型，用 TRPV4特异性抑制剂 HC067047抑制 TRPV4。将培养的 PC12细胞采用随机数字表法分为四组:对照组、 HC067047组、 MPP+组、 HC067047+MPP+组。细胞毒性检测试剂盒( CCK-8)检测各组细胞的增殖活力。蛋白印迹法和酶联免疫吸附测定( ELISA)检测各组细胞 TRPV4和炎症因子白细胞介素 -18(IL-18)、白细胞介素 -6(IL-6)、白细胞介素 -1β(IL-1β)、肿瘤坏死因子 -α(TNF-α)的水平变化。结果与对照组1.00±0.08相比， MPP+组 TRPV4的表达量 2.14±0.20明显升高( P<0.001)。与对照组 1.00±0.01相比， MPP+组的 PC12细胞活力0.65±0.08明显降低( P<0.01)，而 HC067047能明显回复 MPP+引起的细胞活力 0.83±0.07降低( P<0.01)。与对照组相比， MPP+组的 IL-18 1.96±0.27和 IL-6 1.92±0.18、IL-1β(874.61±108.09)ng/L和 TNF-α(791.28±106.88)ng/L明显升高(P<0.001)HC067047能明显抑制 MPP+引起的 IL-18 1.45±0.11和IL-6 1.58±0.22、IL-1β(626.28±84.53)ng/L和 TNF-α(592.94±86.9)4 ng/L明(P<0.01或P<0.05)。结论 TRPV4参与了 MPP+诱导的 PD细胞模型的炎症反应，抑制 TRPV4有抗炎作用。 |
| 英文摘要: |
| Objective To investigate the mechanism of transient receptor potential vanillin receptor subfamily Ⅳ (TRPV4) mediatinginflammation of PC12 cells in Parkinson's disease (PD) cell model.Methods TRPV4 specific inhibitor HC067047 was used to inhibit TRPV4 in 1-methyl-4-phenylpyridinium (MPP+)-induced cell model of Parkinson's disease from June to August 2023. PC12 cells wererandomly divided into four groups: control group, HC067047 group, MPP+ group and HC067047 + MPP+ group. Cell Counting Kit-8 (CCK-8) assays were used to detect the cell viability of each group. The expressions of TRPV4 and the levels of inflammatory factors,such as interleukin (IL)-18, IL-6, IL-1β and tumor necrosis factor -α (TNF-α) were detected by western blot and ELISA.Results Compared with the control group 1.00±0.08, the expression of TRPV4 in MPP+ group 2.14±0.20 was increased (P<0.001). Compared with the control group 1.00±0.01, the cell viability of MPP+ group 0.65±0.08 was decreased obviously (P<0.01), while HC067047 (0.83 ± 0.07) could restore the decrease of cell viability caused by MPP+ (P<0.01). Additionally, the levels of IL-18 1.96±0.27, IL-6 1.92±0.18, IL-1β (874.61±108.09) ng/L and TNF-α (791.28±106.88) ng/L in MPP+ group were increased significantly (P<0.001), while HC067047 could obviously inhibit the high levels of IL-18 1.45±0.11,IL-6 1.58±0.22,IL-1β (626.28±84.53) ng/L and TNF-α (592.94±86.94) ng/L induced by MPP+ (P<0.01 or P<0.05).Conclusion TRPV4 participates MPP+-induced inflammatory response in PD cell model, inhibiting the expression of TRPV4 has anti-inflammatory effect. |
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