Abstract

According to the neuroprotective effects of Zn metal and Elaeagnus angustifolia leaves separately, we tried to synthesize a modern neuroprotective drug (ZnNPs in an aqueous medium by E. angustifolia leaves extract). After ZnNPs synthesizing, they were analyzed by UV-Vis. and FT-IR spectroscopy and FE-SEM. The sizes of 10–50 nm were seen by FE-SEM images in our nanoparticles. In addition, the nanoparticles were spherical morphologically. To investigate the antioxidant effects, DPPH free radicals test was used. The ZnNPs removed half of the free radicals at the 27 µg/mL concentration. In the neurological experiments, we concluded that Nicotine causes cell death in nerve-like PC12 cells by inducing apoptosis and cell inflammation. Zinc nanoparticles repressed the inflammatory cytokines (IL-1β, IL-6, and TNF-α) production, caspase 3 activity, and mitochondrial membrane disruption. These events showed that zinc nanoparticles repressed Nicotine-induced cell death in PC12 cells, in a dose-dependent manner.

摘要

根据锌金属和沙枣叶分别具有的神经保护作用，我们试图合成现代神经保护药物（水性介质中的ZnNPs）。叶提取物）。在 ZnNPs 合成后，通过 UV-Vis 对其进行分析。和 FT-IR 光谱和 FE-SEM。通过我们的纳米粒子中的 FE-SEM 图像可以看到 10-50 nm 的尺寸。此外，纳米颗粒在形态上是球形的。为了研究抗氧化作用，使用了DPPH自由基测试。ZnNPs 在 27 µg/mL 浓度下去除了一半的自由基。在神经学实验中，我们得出结论，尼古丁通过诱导细胞凋亡和细胞炎症导致神经样 PC12 细胞中的细胞死亡。锌纳米颗粒抑制炎症细胞因子（IL-1β、IL-6 和 TNF-α）的产生、半胱天冬酶 3 活性和线粒体膜破坏。这些事件表明，锌纳米颗粒以剂量依赖的方式抑制尼古丁诱导的 PC12 细胞中的细胞死亡。