Ruiting Liu1, Xiaowan Li1. 1. Department of Neurology, Liaocheng People's Hospital Liaocheng 252000, Shandong Province, China.
Abstract
Background: Parkinson's disease (PD) is a degenerative disease of central nervous system. 1-Methyl-4-phenylpyridine (MPP+) is a non-selective dopaminergic neurotoxin that induces cell injury similar to PD. This study aimed to explore the protective effects of Radix Ophiopogonis polysaccharide extracts (ROP) on the MPP+-induced PC-12 cell injury. Methods: PC-12 cells were exposed to MPP+ with or without ROP treatment. Then the cell viability, apoptosis, reactive oxygen species (ROS) level, calcium (Ca2+) concentration, mitochondrial membrane potential (MMP), Cyctochrome C release, mitochondrial ATP synthesis, and the expression level of Notch signaling pathway were detected by CellTiter 96 AQueous One Solution Cell Proliferation assay, fluorescent staining, flow cytometer analysis, and western blotting, respectively. Results: MPP+ treatment obviously induced PC-12 cell injury as evidenced by the cell viability loss and cell apoptosis enhancement. MPP+ markedly increased the concentrations of ROS and Ca2+ and the mitochondrial dysfunction in PC-12 cells. Moreover, the activation of Notch signaling pathway was found after MPP+ treatment. ROP significantly reversed the MPP+-induced PC-12 cell viability loss, apoptosis increase, intracellular oxidative stress and endoplasmic reticulum (ER) stress rise, mitochondrial dysfunction and the activation of Notch signaling pathways in PC-12 cells. Conclusion: ROP protected PC-12 cells from the MPP+-induced injury through suppressing the increase of the intracellular oxidative stress and ER stress and activation of Notch signaling pathway. These findings will be helpful for understanding the protective roles of ROP in nerve cell injury and provide potential therapeutic drug for PD. IJCEP
Background: Parkinson's disease (PD) is a degenerative disease of central nervous system. 1-Methyl-4-phenylpyridine (MPP+) is a non-selective dopaminergic neurotoxin that induces cell injury similar to PD. This study aimed to explore the protective effects of Radix Ophiopogonis polysaccharide extracts (ROP) on the MPP+-induced PC-12 cell injury. Methods:PC-12 cells were exposed to MPP+ with or without ROP treatment. Then the cell viability, apoptosis, reactive oxygen species (ROS) level, calcium (Ca2+) concentration, mitochondrial membrane potential (MMP), Cyctochrome C release, mitochondrial ATP synthesis, and the expression level of Notch signaling pathway were detected by CellTiter 96 AQueous One Solution Cell Proliferation assay, fluorescent staining, flow cytometer analysis, and western blotting, respectively. Results:MPP+ treatment obviously induced PC-12 cell injury as evidenced by the cell viability loss and cell apoptosis enhancement. MPP+ markedly increased the concentrations of ROS and Ca2+ and the mitochondrial dysfunction in PC-12 cells. Moreover, the activation of Notch signaling pathway was found after MPP+ treatment. ROP significantly reversed the MPP+-induced PC-12 cell viability loss, apoptosis increase, intracellular oxidative stress and endoplasmic reticulum (ER) stress rise, mitochondrial dysfunction and the activation of Notch signaling pathways in PC-12 cells. Conclusion: ROP protected PC-12 cells from the MPP+-induced injury through suppressing the increase of the intracellular oxidative stress and ER stress and activation of Notch signaling pathway. These findings will be helpful for understanding the protective roles of ROP in nerve cell injury and provide potential therapeutic drug for PD. IJCEP