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). However, cell viability was unchanged by 10 μmol/L EGCG treatment. In co-treatments with EGCG and MPP+, cell viability was significantly increased by 12.92% (P < 0.05) and MPP+-induced ROS production was markedly decreased. PGC-1α mRNA expression was obviously upregulated by 21.51% (P < 0.05), and SOD1 and GPX1 mRNA expression was slightly increased by 12.94% and 15.63% (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 < 0.05), respectively, by treatment with EGCG and then MPP+ for 24 h. Such effects were not observed with MPP+ treatment alone.ConclusionThe SIRT1/PGC-1α pathway is one of the mechanisms of EGCG suppression of MPP+-induced injury of PC12 cells.

The ionic nature endows halide perovskites with intrinsic interfacial defects in the formed polycrystalline films, thus imposing the challenge of synchronously passivating these defects with low formation energies that directly account for the unsatisfied performance of perovskite solar cells (PSCs). By virtue of the theoretically proven capability of a three to four times enhancement of the formation energy of each defect of Pb‐I antisite (PbI) and iodine vacancy (VI), a new passivation molecule of 1,10‐phenanthrolin‐5‐amine (PAA) is intentionally explored to synchronously passivate the dual defects. The pronounced passivation effect is experimentally verified by the sharp enhancement of the open‐circuit voltage in ternary PSCs from the original 1.118 up to 1.207 V, as well as the construction of PAA‐modified formamidinium lead iodide PSCs with a champion efficiency up to 24.06%, thus providing a universal alternative of addressing interfacial charge carrier dynamics and operational stability of PSCs that are bothered by the multiple interfacial defects.

The rapid growth in the device efficiency of perovskite solar cells (PSCs) has raised great demands for tackling their long-term stability upon external environmental stimuli that restricts the commercialization of PSCs, in which the instability upon exposure to moisture has been one of the major obstacles. Herein, an effective way of building up double barriers for moisture degradation of the perovskite films is demonstrated by modifying them with rationally selected hydrolyzable hydrophobic molecules (1H,1H,2H,2H-perfluorooctyl trichlorosilane, PFTS). The layer of oligomer derived from the hydrolyzed PFTS at the surface that increases the hydrophobicity of perovskite film could serve as an efficient wall preventing the moisture invasion. The long-term exposure of the film upon moisture allows for the formation of a secondary wall that employs the hydrolyzation of PFTS at grain boundaries, favoring defects passivation to further improve the humidity stability. Such gradual hydrolyzation is encouragingly helpful for the enhancement of the open-circuit voltage of the PSCs from the original 1.136 up to 1.205 V. The PSCs constructed with the double barriers demonstrate excellent stability upon moisture and improved thermal and light stabilities, as well as a champion power conversion efficiency up to 21.34%.

These findings demonstrate that both receptor proteins may play an important role in the invasion, metastasis, and recurrence of NPC. Both receptors are valuable markers for assessing the prognosis of NPC. Their expression at such high frequencies provides the basis of combined targeted therapy with specific pharmacologic inhibitors to enhance the effects of radiotherapy and chemotherapy.