2. Academic Validation
  3. The protective effects of the native flavanone flavanomarein on neuronal cells damaged by 6-OHDA

The protective effects of the native flavanone flavanomarein on neuronal cells damaged by 6-OHDA

  • Phytomedicine. 2019 Feb;53:193-204. doi: 10.1016/j.phymed.2018.09.005.
Liang Le 1,  Hui Fu 2,  Qiuyue Lv 2,  Xue Bai 2,  Ying Zhao 2,  Jiamei Xiang 2,  Baoping Jiang 3,  Keping Hu 2,  Shilin Chen 4
Affiliations

Affiliations

  • 1 Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing 100700, China; Post-doctoral Scientific Research Center, China Academy of Chinese Medical Sciences, Beijing 100700, China.
  • 2 Institute of Medicinal Plant Development (IMPLAD), Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100193, China.
  • 3 Institute of Medicinal Plant Development (IMPLAD), Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100193, China. Electronic address: [email protected].
  • 4 Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing 100700, China. Electronic address: [email protected].
PMID: 30668399 DOI: 10.1016/j.phymed.2018.09.005
Abstract

Background: Flavanomarein is the main component of Coreopsis tinctoria Nutt. (C. tinctoria), which is a globally well-known flower tea that has a distinct flavor and many beneficial health effects, such as antioxidant activities. We aimed to explore the effect of flavanomarein on a 6-hydroxydopamine (6-OHDA)-lesioned cell model of oxidative stress.

Methods: In this study, we used 6-OHDA-lesioned PC12 cells and primary cortical neurons to investigate the protective effects of flavanomarein and its potential mechanism.

Results: The results indicated that pretreatment with flavanomarein (25, 50, or 100 µM for 24 h) significantly increased the cell viability, reduced the Lactate Dehydrogenase (LDH) release and improved the mitochondrial membrane potential (∆Ψm) and mitochondrial impairment. Additionally, flavanomarein markedly reduced the gene expression of tumor necrosis factor (TNF)-α and protein kinase C ζ (PKC-ζ), the nuclear translocation of p65, and the levels of p-AMPK-α and acetyl-p53. Flavanomarein also elevated the gene expression of P85α, PKC-β1, and Bcl-2, the protein expression of SIRT1 and ICAD, and the phosphorylation level of Akt.

Conclusions: Together, these results suggest that flavanomarein protects PC12 cells and primary cortical neurons from 6-OHDA-induced neurotoxicity by upregulating the PI3K/Akt signaling pathway and attenuating the nuclear factor kappa B (NF-κB) signaling pathway. Therefore, our study provides evidence that may aid in the development of a potential compound against 6-OHDA toxicity.

Keywords

6-hydroxydopamine; AKT; Flavanomarein; NF-κB; Neuron; PC12 cells.

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