Targeting the Nrf2-dependent mechanism of b-Ecdysterone in attenuating the motor dysfunction in the MPTP/Pro-induced Parkinson's disease mice model.

Oxidative stress is a pivotal stimulating factor in neurocyte apoptosis and has been involved in the pathogenesis of Parkinson's disease (PD). In this study, we have demonstrated that the improvement in the motor disorder of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)/Pro-induced mice caused by b-Ecdysterone (b-Ecd) treatment is due to its antioxidant properties. Using open field, rotarod, and pole climbing tests, we have found that b-Ecd alleviates motor disorder in MPTP/Pro-induced mice and ultimately reduces the impairment of tyrosine hydroxylase (TH)-positive dopaminergic neurons in the substantia nigra (SN). Notably, these effects of b-Ecd were not observed in Nrf2-KO mice. In addition, b-Ecd significantly reduced the formation of ROS and the level of MDA, blocked the increase of LPO, and partially reversed the GSH/GSSG ratio in MPTP/Pro-induced WT mice; however, these results were also not observed in MPTP/Pro-induced Nrf2-KO mice. Mechanistically, b-Ecd enhanced the expression levels of heme oxygenase 1 (HO-1) and GCLc, but not NQO1 (NAD(P)H quinone dehydrogenase 1) and GCLm expression. Interestingly, b-Ecd failed to increase the protein and mRNA levels of HO-1 and GCLc in Nrf2-KO mice, suggesting that b-Ecd attenuates oxidative stress through an Nrf2-dependent mechanism. Furthermore, b-Ecd promoted the expressions of PI3K/Akt phosphorylation (activity) and GSK-3b phosphorylation (inactivity). Conversely, administration of b-Ecd markedly decreased Fyn phosphorylation levels. Collectively, our findings suggest that b-Ecd focuses on Nrf2 in reducing MPTP/Pro-induced oxidative stress and subsequent motor deficits by inhibiting its nuclear export through PI3K/Akt/GSK-3b/Fyn pathway regulation. These further indicate that b-Ecd may be an absorbing therapeutic agent for PD.

Photochemical reduction of CO2 into CO coupling with triethanolamine decomposition.

In this work, the impacts of triethanolamine (TEOA) on the performance of photochemical CO2 reduction were investigated in a simple homogeneous system. We demonstrates that CO2 can be converted into CO coupling with the decomposition of triethanolamine in TEOA aqueous solution without other additives under light irradiation. About 7.5 µmol CO product is achieved within 7 h with a maximum apparent quantum yield (AQY) of 0.086% at 254 nm. The isotope labelling experiment confirms that CO product originates from the reduction of CO2 rather than the decomposition of TEOA. In addition, the photochemical system exhibits excellent stability, no obvious inactivation is observed during long-term photochemical CO2 reduction reaction. This work provides a deep understanding of the effects of TEOA on the performance of photocatalytic CO2 reduction. Upon utilizing TEOA as a sacrificial electron donor in photocatalytic system, the contribution of TEOA must be considered once evaluating the catalytic activity of catalysts.