Controllably partial removal of thiolate ligands from unsupported Au_(25) nanoclusters by rapid thermal treatments for electrochemical CO_(2)reduction

Colloidal synthesis of metal nanoclusters will inevitably lead to the blockage of catalytically active sites by organic ligands.Here,taking[Au_(25)(PET)_(18)]-(PET=2-phenylethanethiol)nanocluster as a model catalyst,this work reports a feasible procedure to achieve the controllably partial removal of thiolate ligands from unsupported[Au_(25)(PET)_(18)]-nanoclusters with the preservation of the core structure.This procedure shortens the processing duration by rapid heating and cooling on the basis of traditional annealing treatment,avoiding the reconfiguration or agglomeration of Au_(25)nanoclusters,where the degree of dethiolation can be regulated by the control of duration.This work finds that a moderate degree of dethiolation can expose the Au active sites while maintaining the suppression of the competing hydrogen evolution reaction.Consequently,the activity and selectivity towards CO formation in electrochemical CO_(2)reduction reaction of Au_(25)nanoclusters can be promoted.This work provides a new approach for the removal of thiolate ligands from atomically precise gold nanoclusters.

Notoginsenoside R1 Protects against Diabetic Nephropathy through TXNIP-NLRP3 Signaling Pathway

Background:Diabetic nephropathy(DN)is a microvascular complication of diabetes mellitus(DM).DN results from many factors,including changes in glomerular hemodynamics,oxidative stress and inflammation,and in-terstitial fibrosis and tubular atrophy.Panax notoginseng,a commonly used Chinese medicine,has been used in the treatment of kidney disease.Notoginsenoside R1(NGR1),the main compound isolated from P.notoginseng,has been reported to have a renoprotective role in DN.However,the therapeutic effect and mechanism of NGR1 in DN remain unclear.Objective:The present study aimed to investigate the therapeutic effect and mechanism of NGR1 in DN.Methods:In this study,mouse podocytes(MPC-5 cells)and db/db mice were used to investigate the effect of NGR1 on DN in vitro and in vivo,respectively.Blood glucose,renal function,inflammatory factors,and PI3K/AKT-Nrf2-NLRP3 signaling pathway proteins were assessed.Results:The study results indicated that NGR1 reversed cell viability induced by high glucose(HG,30 mM).The related mechanism results showed that NGR1 decreased oxidative stress by inhibiting reactive oxygen species(ROS)level and upregulating the expression of Nrf2,NQO1,and HO-1 via TXNIP targeting.In addition,NLRP3 inflammasome and PI3K/AKT were engaged in NGR1-based protection against HG-stimulated podocytes.In db/db mice,NGR1 significantly decreased blood glucose,urine protein,urine output,blood urea nitrogen,and other parameters as well as reversed kidney injury by inhibiting oxidative stress and proinflammatory response.Conclusion:Taken together,this study revealed that NGR1 exerted a significant therapeutic effect on DN both in vitro and in vivo via a mechanism related to the TXNIP-Nrf2 pathway and NLRP3 inflammasome,suggesting that NGR1 is a potential therapeutic option for DN.

Photodynamic Therapy Activities of 10-（4-Formylphenyl）-5,15-bis（pentafluorophenyl）corrole and Its Gallium Complex

10-（4-Formylphenyl）-5,15-bis（pentafluorophenyl）corrole 1 and its gallium complex 1-Ga were used to investigate their photocytotoxicity in liver cancer （BEL-7402）, lung cancer （A549） and cervical cancer （Siha, Hela） cell lines. Among all the tested tumor cells, Siha tumor cells were the most sensitive to photodynamic therapy （PDT） treatment by 1 and 1-Ga. PDT IC50 of 1 and 1-Ga toward Siha tumor cell reaches 1.3 and 0.8 gmol/L respectively, which is 10-fold higher than that of cisplatin. 1 and 1-Ga might pass across the tumor cell membrane smoothly without the help of carrier protein, and mainly localized in the cytoplasm of tumor cell. After PDT treatment, the intracellular reactive oxygen species （ROS） level increased and the mitochondrial membrane potential decreased significantly, which would finally result in the apoptosis of tumor cells.