Notoginsenoside R1 Promotes the Growth of Neonatal Rat Cortical Neurons via the Wnt/β-catenin Signaling Pathway

Author:

Li Xing-Tong1,Ma Wei1,Wang Xian-Bin1,Liang Zhang1,Yang Jin-Wei1,He Yuan2,Dai Yun-Fei1,Zhang Tong3,Wang Jia-Wei3,Liu Kuang-Pin1,Wang Xiang-Peng1,Zhang Xing-Kui1,Li Chun-Yan1,Li Jun-Jun1,Tang Hong-Yan4,Su Ping5,Guo Jian-Hui3,Li Li-Yan1

Affiliation:

1. Institute of Neuroscience, Kunming Medical University, Yunnan Kunming, China

2. Department of Gastroenterology, First People`s Hospital of Yunnan Province, Yunnan Kunming, China

3. Second Department of General Surgery, First People`s Hospital of Yunnan Province, Yunnan Kunming, China

4. Department of Neurosurgery, First Affiliated Hospital of Kunming Medical University, Yunnan Kunming, China

5. Department of Neurosurgery, First People`s Hospital of Kunming City, Yunnan Kunming, China

Abstract

Background & Objective: Notoginsenoside R1 (NGR1) is one of the main effective components of Panax notoginseng. Method: Primary cortical neurons were harvested from neonatal rats and cultured to analyze the role of NGR1 in neuronal growth and the effects of NGR1 on the Wnt/β-catenin signaling pathway. Following treatment with NGR1, immunocytochemistry was used to detect expression of Tuj1 and MAP2, and RT-qPCR was used to measure mRNA levels of key factors in the Wnt signaling pathway. Results: Results showed that NGR1 promotes growth of cultured neurons and significantly upregulates mRNA levels of β-catenin, Dishevelled, and Frizzled. To further confirm whether NGR1 promoted cortical neuron growth via the Wnt/β-catenin signaling pathway, we knocked down β- catenin mRNA by siRNA interference; following NGR1 treatment of β-catenin-knockdown neurons, β-catenin mRNA levels increased significantly. Conclusion: In conclusion, these results demonstrate that NGR1 promotes growth of cultured cortical neurons from the neonatal rat, possibly via the Wnt/β-catenin signaling pathway.

Publisher

Bentham Science Publishers Ltd.

Subject

Pharmacology,General Neuroscience

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