International Journal of Pharmacology

Volume 18 (6), 1309-1321, 2022

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Influence of Nervonic Acid on Parkinson’s Disease Model Cells through Ras/MEK/ERK Axis

Dandong Hu, Yujuan Cui and Ji Zhang

Background and Objective: Parkinson’s disease (PD) is currently the most common disease with a high incidence worldwide. However, there are few studies regarding the role of neuronic acid (NA) in PD. So this study aimed to explore the intervention effect of NA and further understand its influence on the disease to provide a reliable theoretical basis for future clinical practice. Materials and Methods: Human neuroblastoma cells (SH-SY5Y) and adrenal pheochromocytoma (PC-12) were induced to establish PD cell models, which were assigned to high- (20 μmol L1 NA), medium- (10 μmol L1 NA) and low-dose (5 μmol L1 NA) groups, as well as model group (normal saline intervention) respectively. Normal SH-SY5Y and PC-12 were used as controls. Levels of oxidative stress (OS) and inflammation in cells were measured by PCR and lactate dehydrogenase (LDH) release was analyzed. Western blot was used to determine Ras/MEK/ERK axis-related protein expression and apoptosis. Results: Inflammatory factors (IFs) and OS were inhibited and LDH release decreased in the three groups of cells intervened by NA. In addition, the model group showed markedly enhanced apoptosis, while NA intervened cells presented reduced apoptosis and increased Ras/MEK/ERK axis-related protein expression. After inhibiting the Ras/MEK/ERK axis, the oxidative stress response (OSR), IFs, LDH release and apoptosis of PD cells increased obviously. In the rescue experiment, inhibiting the Ras/MEK/ERK axis completely reversed NA’s effects on PD model cells. Conclusion: NA suppresses PD cell apoptosis via activating the Ras/MEK/ERK axis and alleviates the OS injury and inflammatory damage of cells.

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How to cite this article:

Dandong Hu, Yujuan Cui and Ji Zhang, 2022. Influence of Nervonic Acid on Parkinson’s Disease Model Cells through Ras/MEK/ERK Axis. International Journal of Pharmacology, 18: 1309-1321.

DOI: 10.3923/ijp.2022.1309.1321

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