论文部分内容阅读
Objective: To evaluate the protective effect of peanut sprout extract(PSE) against paraquat(PQ) induced SK-N-SH cells.Methods: Three groups of cells were used in the experiment, together with a fourth,control group. One group was treated with PQ, the second group was treated with PSE,and the third group was pre-treated with PSE. The control group was untreated. Cell viability and toxicity were detected by MTT assay, cellular reactive oxygen species(ROS) was detected by Muse Cell Analyzer, quantitative RT-PCR was applied to investigate the expression of SIRT1 and a-synuclein genes, and A b42 was detected by western blot.Results: The 50% effective concentration of PQ was 0.75 mmol/L. PSE had no significant cytotoxicity at a concentration of 1.5 mg/m L. In the group of cells pre-treated with PSE, cell death was significantly inhibited. In the PQ treated group, PQ was increased in the intracellular ROS in the cells. Intracellular ROS was significantly decreased in the cells treated with PSE and also those pre-treated with PSE. PSE significantly downregulated the expression of SIRT1 and a-syn genes, and it was found that PQ significantly increased b-amyloid 42 levels whereas this action was inhibited by PSE.Conclusions: PSE has neuroprotective activities against oxidative stress in SK-N-SH cells induced by PQ, suggesting that PSE is a highly promising agent in the prevention of neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease.
Objective: To evaluate the protective effect of peanut sprout extract (PSE) against paraquat (PQ) induced SK-N-SH cells. Methods: Three groups of cells were used in the experiment, together with a fourth, control group. One group was The control group was untreated. Cell viability and toxicity were detected by MTT assay, cellular reactive oxygen species (ROS) was detected by Muse Cell Analyzer, quantitative RT-PCR was applied to investigate the expression of SIRT1 and a-synuclein genes, and A b42 was detected by western blot. Results: The 50% effective concentration of PQ was 0.75 mmol / L. PSE had no significant cytotoxicity At a concentration of 1.5 mg / m L. In the group of cells pre-treated with PSE, cell death was significantly inhibited. PQ treated group, PQ was increased in the intracellular ROS in the cells. the cells treated with PS E and also those pre-treated with PSE. PSE significantly downregulated the expression of SIRT1 and a-syn genes, and it was found that PQ significantly increased b-amyloid 42 levels and this action was inhibited by PSE. Conclusions: PSE has neuroprotective activities suggesting oxidative stress in SK-N-SH cells induced by PQ, suggesting that PSE is a highly promising agent in the prevention of neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease.