Effect of Protocatechuic Acid on Preventing PC12 Cells from Aamyloid Beta-Peptide-induced Toxicity and Its Mechanism
10.13359/j.cnki.gzxbtcm.2016.01.017
- VernacularTitle:原儿茶酸对β淀粉样蛋白1-42诱导PC12细胞毒性的保护作用及机制
- Author:
Ruwei DAI
;
Shijie ZHANG
;
Weibin CAI
;
Huifang CHEN
;
Na ZHENG
;
Qingqing XU
;
Yifan ZHANG
;
Qi WANG
- Publication Type:Journal Article
- Keywords:
protocatechuic acid/pharmacology;
Alzheimer’s disease/TCD therapy;
PC12 cells/pathology;
cell culture;
protein expression
- From:
Journal of Guangzhou University of Traditional Chinese Medicine
2016;(1):66-70
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective effect of protocatechuic acid(PCA)on the PC12 cell model of Alzheimer’s disease(AD)and to explore its mechanism . Methods Amyloid beta peptide 1-42(Aβ1-42)fiber polymers were identified by immunofluorescence. After PC12 cells were stimulated with the Aβ1-42 fiber polymers, the cellular morphology was observed at different time points of hour 0, 3, 6, 9, 12, 24 , and the cellular viability was tested by methyl thiazolyl tetrazolium(MTT)assay to monitor the modeling condition. The effect of PCA on PC12 cells was detected after PC12 cells were pretreated with the different contentions of PCA. Autophagy-related marker Beclin1 protein level was detected by Western blotting method to investigate the protective mechanism of PCA. Results Aggregated white Aβ1-42 mass was stable at hour 12 and 24, and showed no significant difference between the two time points, the cell damage rate being 40%. Therefore, we defined culturing time being 12 and 24 hours as the modeling condition of AD model. The cell viability was increased with 200-800 μmol/L of PCA after culturing for 24 hours(P<0.01) , and the Western blotting results showed that the Beclin1 protein expression was up-regulated by PCA. Conclusion PCA prevents PC12 cells from Aβ1-42-induced toxicity, the mechanism being related with the increase of cellular autophagy.
