藏红花黄A通过Nrf2/HO-1通路对h2o2诱导的PC12细胞氧化应激损伤的保护作用

IF 0.6 4区 医学 Q4 CHEMISTRY, MEDICINAL
Hui Chen, Sichun Gu, Yi You, Anjie Xie, Yiying Lu, Changde Wang
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The detection method is 5-(and 6)-chloromethyl-2′,7′-dichloro-dihydrofluorescein diacetate (CM-H2DCF-DA) staining reactive oxygen species (ROS). Levels of apoptosis-related proteins, including Bcl2-associated X protein (Bax), B-cell lymphoma (Bcl-2), caspase-3, and cleaved caspase-3, and oxidative stress regulators, namely, nuclear factor erythroid-2-related actor 2 (Nrf2) and heme oxygenase 1 (HO-1), were detected by western blotting. Results The CCK-8 assay results showed that the survival rate of H 2 O 2 -induced PC12 cells was significantly increased after SYA treatment. Fluorescence microscopy (CM-H2DCF-DA staining) indicated that SYA decreased H 2 O 2 -induced apoptosis in PC12 cells by reducing intracellular ROS. Western blotting analysis showed that SYA upregulated the expression of Nrf2, HO-1, and Bcl-2 and downregulated the expression of Bax, caspase 3, and cleaved caspase-3 in H 2 O 2 -induced PC12 cells. 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引用次数: 0

摘要

红花黄(Safflor yellow, SY)是干花中的一种容水性成分,主要来自红花科的红花,含有大量的芽素a,简称红花黄a (SYA)。研究报道了SYA对神经细胞氧化应激损伤的保护作用。本研究以h2o2处理的PC12细胞为实验材料,探讨SYA对氧化应激后神经细胞的保护作用,并分析SYA的分子机制。用h2o2和SYA溶液处理PC12细胞。然后用细胞计数试剂盒-8 (CCK-8)检测细胞增殖。检测方法为5-(和6)-氯甲基-2′,7′-二氯-双氢荧光素(CM-H2DCF-DA)染色活性氧(ROS)。western blotting检测凋亡相关蛋白,包括bcl2相关X蛋白(Bax)、b细胞淋巴瘤(Bcl-2)、caspase-3和cleaved caspase-3,以及氧化应激调节因子,即核因子红细胞2相关因子2 (Nrf2)和血红素加氧酶1 (HO-1)的水平。结果CCK-8实验结果显示,SYA处理后h2o2诱导的PC12细胞存活率显著提高。荧光显微镜(CM-H2DCF-DA染色)显示,SYA通过减少细胞内ROS来减少h2o2诱导的PC12细胞凋亡。Western blotting分析显示,SYA上调h2o2诱导的PC12细胞中Nrf2、HO-1和Bcl-2的表达,下调Bax、caspase 3和cleaved caspase-3的表达。结论SYA具有保护神经细胞免受氧化应激损伤的作用。其作用机制主要与Nrf2/HO-1通路是否被激活有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Protective Effects of Safflor Yellow A Against H2O2-induced Oxidative Stress Injury in PC12 Cells via Nrf2/HO-1 Pathway
Background Safflor yellow (SY) is a water-capacitive component of dried flowers, mainly from safflor in the safflower family, which contains a large amount of bruthin A, or Safflor yellow A (SYA) for short. Studies have reported the protective effects of SYA against oxidative stress injury in nerve cells. Materials and Methods In this study, H 2 O 2 -treated PC12 cells were used as experimental materials to explore how SYA plays a protective role against nerve cells after oxidative stress and to analyze the molecular mechanism of SYA. PC12 cells were treated with H 2 O 2 and SYA solution. Cell proliferation is then detected with Cell Counting Kit-8 (CCK-8). The detection method is 5-(and 6)-chloromethyl-2′,7′-dichloro-dihydrofluorescein diacetate (CM-H2DCF-DA) staining reactive oxygen species (ROS). Levels of apoptosis-related proteins, including Bcl2-associated X protein (Bax), B-cell lymphoma (Bcl-2), caspase-3, and cleaved caspase-3, and oxidative stress regulators, namely, nuclear factor erythroid-2-related actor 2 (Nrf2) and heme oxygenase 1 (HO-1), were detected by western blotting. Results The CCK-8 assay results showed that the survival rate of H 2 O 2 -induced PC12 cells was significantly increased after SYA treatment. Fluorescence microscopy (CM-H2DCF-DA staining) indicated that SYA decreased H 2 O 2 -induced apoptosis in PC12 cells by reducing intracellular ROS. Western blotting analysis showed that SYA upregulated the expression of Nrf2, HO-1, and Bcl-2 and downregulated the expression of Bax, caspase 3, and cleaved caspase-3 in H 2 O 2 -induced PC12 cells. Conclusion SYA does protect the nerve cells from oxidative stress damage. Its mechanism of action is mainly related to whether the Nrf2/HO-1 pathway is activated.
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来源期刊
Pharmacognosy Magazine
Pharmacognosy Magazine CHEMISTRY, MEDICINAL-
CiteScore
1.87
自引率
0.00%
发文量
37
审稿时长
3 months
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