Epigallocatechin-3-gallat, PC12 hücrelerinde 1-metil-4-fenil-piridin kaynaklı oksidatif stresi SIRT1/PGC-1 ⁇ sinyal yolu ile bastırır.

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BackgroundParkinson's disease is a high incidence neurodegenerative disease in elderly people, and oxidative stress plays an important role in the pathogenesis. Oxygen metabolism in the brain is high, which lacks an antioxidative protection mechanism. Recently, it has been found that polyphenols play an important role in antioxidation. (-)-epigallocatechin-3-gallate (EGCG) is an important component of tea polyphenols and its biological effects, such as strong antioxidation, scavenging of free radicals and anti-apoptosis, can pass through the blood brain barrier. The SIRT1/PGC-1α signaling pathway has not been reported in PC12 cells. Therefore, research of the protective mechanism of EGCG in PC12 cells damaged by -methyl-4-phenyl-pyridine (MMP+) may provide a new insight into protect against and treatment of Parkinson's disease.MethodsMPP(+)-treated highly differentiated PC12 cells were used as the in vitro cell model. An MTT assay was used to investigate cell viability after EGCG treatment, a dichlorofluorescin diacetate assay was used to measure reactive oxygen species (ROS) production, western blot analysis was used to observe PGC-1α and SIRT1 protein expression, and real-time PCR to observe PGC-1α, SOD1 and GPX1 mRNA expression.ResultsPC12 cell viability was significantly reduced after MPP(+) treatment by 11.46% compared with that of the control (P 0.05), respectively, by treatment with EGCG and then MPP(+) for 12 h. The mRNA expression of PGC-1α, SOD1 and GPX1 was increased by 25.17%, 40% and 146% (all P ConclusionThe SIRT1/PGC-1α pathway is one of the mechanisms of EGCG suppression of MPP(+)-induced injury of PC12 cells.

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