http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Antioxidant Effects of Pyrogallol in Neural Cells and Mice Brain
문지섭(Jisub Moon),곽희선(Heesun Gwak),이태희(Tae-Hee Lee),안은석(Eun Suk An),김윤배(Yun-Bae Kim),박동선(Dongsun Park) 한국교원대학교 뇌기반교육연구소 2019 Brain, Digital, & Learning Vol.9 No.3
Polyphenols can easily react with reactive oxygen species (ROS) resulting in powerful antioxidant activity. Pyrogallol is a polyphenol found in a variety of fruits and vegetables. Therefore, plants containing pyrogallol can be used for their antioxidant, anti-bacterial, anti-fungal, anti-allergic, and anti-inflammatory properties. However, its effectiveness as an antioxidant is still a matter of debate because pyrogallol is also a superoxide anion generator and induces superoxide anion-mediated death of several types of cells. In this study, we tried to confirm the antioxidant effects and mechanisms of pyrogallol in mouse neuroblastoma (N2A), human neural stem cells (F3), and mouse brain. Treatments with various concentrations of pyrogallol significantly increased the free radical scavenging ability and reduced lipid peroxidation in N2A and F3 cells in a concentration-dependent manner. In the cytotoxicity test, low concentrations of pyrogallol (0–10 µg/mL) did not significantly influence cell viability, while high concentrations (125-1000 µg/mL) induced death in N2a and F3 cells. Furthermore, treatment with pyrogallol(1.0, 3.2, and 10.0 µg/mL) up-regulated the mRNA expression of superoxide dismutases 1, 2, and 3, glutathione peroxidase (GPx)1, and phospholipid hydroperoxide GPx in N2A and F3 cells, in the brains of mice that were orally administered pyrogallol (1.0, 3.2, and 10.0 mg/kg/day) for 7 days. The mice did not exhibit any toxic effects due to this treatment. Taken together, although pyrogallol induced cell death at high concentrations, it might be a good candidate antioxidant for neurodegenerative disease at low concentrations.
Komakech, Alfred,Im, Ji-Hye,Gwak, Ho-Shin,Lee, Kyue-Yim,Kim, Jong Heon,Yoo, Byong Chul,Cheong, Heesun,Park, Jong Bae,Kwon, Ji Woong,Shin, Sang Hoon,Yoo, Heon The Korean Neurosurgical Society 2020 Journal of Korean neurosurgical society Vol.63 No.5
Objective : Radiation is known to induce autophagy in malignant glioma cells whether it is cytocidal or cytoprotective. Dexamethasone is frequently used to reduce tumor-associated brain edema, especially during radiation therapy. The purpose of the study was to determine whether and how dexamethasone affects autophagy in irradiated malignant glioma cells and to identify possible intervening molecular pathways. Methods : We prepared p53 mutant U373 and LN229 glioma cell lines, which varied by phosphatase and tensin homolog (PTEN) mutational status and were used to make U373 stable transfected cells expressing GFP-LC3 protein. After performing cell survival assay after irradiation, the IC<SUB>50</SUB> radiation dose was determined. Dexamethasone dose (10 μM) was determined from the literature and added to the glioma cells 24 hours before the irradiation. The effect of adding dexamethasone was evaluated by cell survival assay or clonogenic assay and cell cycle analysis. Measurement of autophagy was visualized by western blot of LC3-I/LC3-II and quantified by the GFP-LC3 punctuated pattern under fluorescence microscopy and acridine orange staining for acidic vesicle organelles by flow cytometry. Results : Dexamethasone increased cell survival in both U373 and LN229 cells after irradiation. It interfered with autophagy after irradiation differently depending on the PTEN mutational status : the autophagy decreased in U373 (PTEN-mutated) cells but increased in LN229 (PTEN wild-type) cells. Inhibition of protein kinase B (AKT) phosphorylation after irradiation by LY294002 reversed the dexamethasone-induced decrease of autophagy and cell death in U373 cells but provoked no effect on both autophagy and cell survival in LN229 cells. After ATG5 knockdown, radiation-induced autophagy decreased and the effect of dexamethasone also diminished in both cell lines. The diminished autophagy resulted in a partial reversal of dexamethasone protection from cell death after irradiation in U373 cells; however, no significant change was observed in surviving fraction LN229 cells. Conclusion : Dexamethasone increased cell survival in p53 mutated malignant glioma cells and increased autophagy in PTEN-mutant malignant glioma cell but not in PTEN-wildtype cell. The difference of autophagy response could be mediated though the phosphatidylinositol 3-kinase/AKT/mammalian target of rapamycin signaling pathway.