School of Pharmacy, Lanzhou University, No.199 Donggang West Road, Lanzhou, Gansu, 730000, China; Frontiers Science Center for Rare Isotopes, No.222 Tianshui South Road, Lanzhou, Gansu, 730000, China.
School of Pharmacy, Lanzhou University, No.199 Donggang West Road, Lanzhou, Gansu, 730000, China.
J Ethnopharmacol. 2023 Nov 15;316:116741. doi: 10.1016/j.jep.2023.116741. Epub 2023 Jun 6.
Shenqi formula is composed of Codonopsis pilosula (Cp) and Lycium barbarum (Lb), and it is traditionally used for promoting qi and nourishing the spleen, liver and kidney. Cp and Lb have been reported to improve cognitive performance in APP/PS1 mice, prevent the accumulation of Aβ, and reduce the neurotoxicity of Aβ to achieve the anti-Alzheimer's disease (AD) effect.
Shenqi formula was explored the therapeutic effect on Caenorhabditis elegans AD pathological model and the underlying mechanism of action.
Paralysis assay and serotonin sensitivity assay was used to detect whether Shenqi formula can alleviate AD paralysis phenotype, and then DPPH, ABTS, NBT and Fenton methods were applied to investigate the scavenging capacity to free radical, ROS, ·O and ·OH of Shenqi formula in vitro. HDCF-DA and MitoSOX™ Red were employed to measure ROS and O accumulation, respectively. RNAi was used to knock down the expression of skn-1 and daf-16 related to oxidative stress resistance signalling pathway. Fluorescence microscopy was used to record the expression of SOD-3::GFP, GST-4::GFP, SOD-1::YFP, and the nuclear translocation of SKN-1 and DAF-16. Western blot assay was carried out to test Aβ monomers and oligomers.
Shenqi formula delayed the AD-like pathological characteristics in C. elegans, and the complete Shenqi formula was more effective than Cp or Lb alone. The effect of Shenqi formula on delaying worm paralysis was partially eliminated by skn-1 RNAi, but not daf-16 RNAi. Shenqi formula significantly inhibited the abnormal deposition of Aβ protein, decreased Aβ protein monomers and oligomers. It increased the expressions of gst-4, sod-1, and sod-3 similar to paraquat, companied by rise then fall of ROS and O in AD worms.
Shenqi formula at least partially depended on SKN-1 signalling pathway to exert its anti-AD effect, and it is potential to be used as a kind of health food to prevent the progress of AD.
参芪方由党参（Cp）和枸杞（Lb）组成，传统上用于补气、健脾、养肝、补肾。已有报道称，Cp 和 Lb 可改善 APP/PS1 小鼠的认知表现，防止 Aβ 的积累，并降低 Aβ 的神经毒性，从而达到抗阿尔茨海默病（AD）的效果。
探讨参芪方对秀丽隐杆线虫 AD 病理模型的治疗作用及其作用机制。
采用麻痹试验和血清素敏感性试验检测参芪方是否能缓解 AD 麻痹表型，然后采用 DPPH、ABTS、NBT 和 Fenton 法测定参芪方在体外对自由基、ROS、·O 和·OH 的清除能力。采用 HDCF-DA 和 MitoSOX™ Red 分别测定 ROS 和 O 的积累。采用 RNAi 敲低与氧化应激抵抗信号通路相关的 skn-1 和 daf-16 的表达。荧光显微镜用于记录 SOD-3::GFP、GST-4::GFP、SOD-1::YFP 的表达以及 SKN-1 和 DAF-16 的核转位。采用 Western blot 法检测 Aβ 单体和寡聚体。
参芪方延缓了秀丽隐杆线虫的 AD 样病理特征，且完整的参芪方比 Cp 或 Lb 单独使用更有效。参芪方对延缓蠕虫麻痹的作用部分被 skn-1 RNAi 消除，但 daf-16 RNAi 没有消除。参芪方显著抑制 Aβ 蛋白的异常沉积，减少 Aβ 蛋白单体和寡聚体。它增加了 gst-4、sod-1 和 sod-3 的表达，类似于百草枯，伴随着 AD 蠕虫中 ROS 和 O 的先升后降。
参芪方至少部分通过 SKN-1 信号通路发挥其抗 AD 作用，有望作为一种保健品，防止 AD 的进展。
