Abstract Title:

The study of neuroprotective effect of ferulic acid based on cell metabolomics.

Abstract Source:

Eur J Pharmacol. 2019 Sep 26:172694. Epub 2019 Sep 26. PMID: 31563648

Abstract Author(s):

Chun-Li Yin, Ri-Gang Lu, Jin-Fang Zhu, Hong-Jia Zhu, Xi Liu, Qiao-Feng Li, Yi-Yi Mo, Hui-Min Huang, Bonnie Chin, Jin-Xia Wu, Xu-Wen Liu, Bang Cheng, Jun-Xiang Ruan, Yong-Hong Liang, Hui Song, Hua Zheng, Hong-Wei Guo, Zhi-Heng Su

Article Affiliation:

Chun-Li Yin


Ferulic acid (FA), a naturally derived phenolic compound, has antioxidant and antidepressant-like effects. It is still a challenge to study its mechanism due to the complexity of the pathophysiology of depression. In this study, ultra-high performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-QTOF-MS) was used to perform metabolomics studies based on biochemical changes in differentiated rat pheochromocytoma (PC12) cells treated with corticosterone-induced neurological damage after FA treatment. A total of 31 metabolites were identified as potential biomarkers for corticosterone-induced PC12 cells injury. Among them, 24 metabolites were regulated after FA treatment. Pathway analysis revealed that these metabolites were mainly involved in the amino acid metabolism, energy metabolism and glycerophospholipid metabolism. In addition, based on the results of metabolomics, three cell signaling pathways related to glutamate were discovered. To further study the interactions between FA and major targets in three signaling pathways, a molecular docking method was employed. The results showed that FA had the strongest binding power with protein kinase B (AKT). Furthermore, the result ofmRNA changes analyzed by quantitative real time RT-PCR indicated that AKT and protein kinase A (PKA) in the signaling pathway were up regulated after treatment with FA compared with model group. This study shows that strategies based on cell metabolomics associated with molecular docking and molecular biology is a helpful tool to elucidate the neuroprotective mechanism of FA.

Study Type : In Vitro Study

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