1. Academic Validation
  2. Notoginsenoside R2 reduces A β 25-35-induced neuronal apoptosis and inflammation via miR-27a/SOX8/ β-catenin axis

Notoginsenoside R2 reduces A β 25-35-induced neuronal apoptosis and inflammation via miR-27a/SOX8/ β-catenin axis

  • Hum Exp Toxicol. 2021 Dec;40(12_suppl):S347-S358. doi: 10.1177/09603271211041996.
Yueqiang Hu 1 2 Lin Wu 1 2 3 Lingfei Jiang 4 Ni Liang 1 Xiaomin Zhu 4 Qianchao He 1 Hongling Qin 1 Wei Chen 1 2
Affiliations

Affiliations

  • 1 Department of Neurology, 118330The First Affiliated Hospital of Guangxi University of Chinese Medicine, Nanning, China.
  • 2 Guangxi Key Laboratory of Chinese Medicine Foundation Research, Guangxi University of Chinese Medicine, Nanning, China.
  • 3 Scientific Laboratorial Centre, Guangxi University of Chinese Medicine, Nanning, China.
  • 4 Graduate College of Guangxi University of Traditional Chinese Medicine, Nanning, China.
Abstract

Background: Alzheimer's disease (AD) has affected numerous elderly individuals worldwide. Panax notoginseng has been shown to ameliorate AD symptoms, and notoginsenoside R2 is a key saponin identified in this plant. Purpose: In the current study, we aimed to explore whether notoginsenoside R2 could improve the prognosis of AD. Methods: Herein, primary rat cortical neurons were isolated and they were treated with amyloid beta-peptide (Aβ) 25-35 oligomers. Cellular Apoptosis was examined via flow cytometry and Western blotting. miR-27a and SOX8 mRNA expression levels were quantified by quantitative reverse transcription-polymerase chain reaction. Furthermore, the interaction between miR-27a and SOX8 was investigated by utilizing a dual-luciferase reporter assay. Finally, an AD mouse model was established to validate the in vitro findings. Results: Notoginsenoside R2 alleviated Aβ25-35-triggered neuronal Apoptosis and inflammation. During this process, miR-27a expression was decreased by notoginsenoside R2, and miR-27a negatively modulated SOX8 expression. Furthermore, activation of SOX8 upregulated β-catenin expression, thus suppressing Apoptosis and neuroinflammation. Conclusions: Our animal experiments revealed that notoginsenoside R2 enhanced the cognitive function of AD mice and inhibited neuronal Apoptosis. Notoginsenoside R2 ameliorated AD symptoms by reducing neuronal Apoptosis and inflammation, thus suggesting a novel direction for AD pharmacotherapy.

Keywords

Alzheimer’s disease; Notoginsenoside R2; SOX8; miR-27a.

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