Ag/AgBr-oxygen enriched g-C3N4 for efficient photocatalytic degradation of trimethylamine.

In this study, Ag/AgBr-O-gCN samples with ternary Z-type heterojunctions were prepared by in situ photoreduction using water as the reducing agent for generating Ag/AgBr active species and oxygen doping. The experimental results indicated that Ag/AgBr-O-gCN degraded trimethylamine by nearly 100% in half an hour and maintained 90% of its original activity after five cycles. The kinetic constant of Ag/AgBr-O-gCN was excellent at 0.0928 min-1, 3.8 times that of gCN, 2.3 times that of Ag/AgBr-gCN, and 1.9 times that of O-gCN. Unlike Ag/AgBr-gCN photoreduced by methanol, gCN was used as an electron donor in the aqueous solution during the photoreduction process, and oxidation sites between the gCN skeleton and Ag/AgBr were formed for constructing the heterojunction system. The Z-type heterojunction system was established by introducing a suitable size of Ag nanoparticles as the recombination center to keep indirect contact between gCN and AgBr. This effectively reduced the electron-hole recombination rate and caused activity enhancement. This study offers a novel idea for the construction of a ternary heterojunction.

Epigenetic control of circadian clocks by environmental signals.

Circadian clocks have evolved to enable organisms to respond to daily environmental changes. Maintaining a robust circadian rhythm under various perturbations and stresses is essential for the fitness of an organism. In the core circadian oscillator conserved in eukaryotes (from fungi to mammals), a negative feedback loop based on both transcription and translation drives circadian rhythms. The expression of circadian clock genes depends both on the binding of transcription activators at the promoter and on the chromatin state of the clock genes, and epigenetic modifications of chromatin are crucial for transcriptional regulation of circadian clock genes. Herein we review current knowledge of epigenetic regulation of circadian clock mechanisms and discuss how environmental cues can control clock gene expression by affecting chromatin states.

Cell Membrane-Targeting Type I/II Photodynamic Therapy Combination with FSP1 Inhibition for Ferroptosis-Enhanced Photodynamic Immunotherapy.

An imbalance in reactive oxygen species (ROS) levels in tumor cells can result in the accumulation of lipid peroxide (LPO) which can induce ferroptosis. Moreover, elevated ROS levels in tumors present a chance to develop ROS-based cancer therapeutics including photodynamic therapy (PDT) and ferroptosis. However, their anticancer efficacies are compromised by insufficient oxygen levels and inherent cellular ROS regulatory mechanism. Herein, a cell membrane-targeting photosensitizer, TBzT-CNQi, which can generate 1O2, •OH, and O2 •- via type I/II process to induce a high level of LPO for potent ferroptosis and photodynamic therapy is developed. The FSP1 inhibitor (iFSP1) is incorporated with TBzT-CNQi to downregulate FSP1 expression, lower the intracellular CoQ10 content, induce a high level of LPO, and activate initial tumor immunogenic ferroptosis. In vitro and in vivo experiments demonstrate that the cell membrane-targeting type I/II PDT combination with FSP1 inhibition can evoke strong ICD and activate the immune response, which subsequently promotes the invasion of CD8+ T cells infiltration, facilitates the dendritic cell maturation, and decreases the tumor infiltration of tumor-associated macrophages. The study indicates that the combination of cell membrane-targeting type I/II PDT and FSP1 inhibition holds promise as a potential strategy for ferroptosis-enhanced photodynamic immunotherapy of hypoxia tumors.

NIR-II Emissive Superoxide Radical Photogenerator for Photothermal/Photodynamic Therapy against Hypoxic Tumor.

Due to the "Achilles' heels" of hypoxia, complicated location in solid tumor, small molecular photosensitizers with second near-infrared window (NIR-II) fluorescence, type-I photodynamic therapy (PDT), and photothermal therapy (PTT) have attracted great attention. However, these photosensitizers are still few but yet challenging. Herein, an "all in one" NIR-II acceptor-donor-acceptor fused-ring photosensitizer, Y6-Th, is presented for the in-depth diagnosis and efficient treatment of cancer. Benefiting from the strong intramolecular charge transfer, promoted highly efficient intersystem crossing, largely p-conjugated fused-ring structure, and reduced planarity, the fabricated nanoparticles (Y6-Th nanoparticles) can emit NIR-II fluorescence with the peak located at 1020 nm, exclusively generate O2•- for type-I PDT, and display excellent PTT performance under an 808 nm laser stimulation. These characteristics make Y6-Th a distinguished NIR-wavelength-triggered phototheranostic agent, which can effectively therapy the hypoxic tumor using NIR-II-fluorescence-guided type-I PDT/PTT. This work provides a valuable guideline for fabricating high-performing NIR-II emissive superoxide radical photogenerators.

Tartary buckwheat root polysaccharides ameliorate non-alcoholic fatty liver disease via the IL6-SOCS3-SREBP1c pathway.

Our previous study demonstrated that Tartary buckwheat root polysaccharides (TBRP) could reduce insulin resistance in diabetes mellitus by inhibiting SOCS3-stimulated IRS1 protein degradation. However, whether TBRP has the efficiency to treat non-alcoholic fatty liver disease (NAFLD) is still undetermined. This investigation aimed to examine the effects of TBRP on a high-fat diet (HFD)-triggered NAFLD, and elucidate the underlying molecular mechanisms. Briefly, TBRP toxicity in hepatoma (BEL7404) and pancreatic cancer (BxPC3) cells and zebrafish embryos developmental models, were evaluated in-vitro and in-vivo, respectively. TBRP inhibited cellular lipid accumulation by suppressing fat synthesis, furthermore, it improved body weight gain, liver weight, liver-to-body weight ratio, serum lipids triglyceride, total cholesterol, ALT, LDL-C, HDL-C, and AST levels in the NAFLD mice model. Additionally, TBRP treatment also lowered the nitric oxide content. The qPCR assay revealed that mRNA expression of TNF, IL1ß, and IL6 was also markedly reduced in TBRP-treated NAFLD mice. The expression of SOCS3, SREBP1c, and STAT3 was elucidated by western blot analysis, which indicated that TBRP markedly decreased the gene expression for de novo fat synthesis by the SOCS3-SREBP1c pathway. These findings reveal that TBRP ameliorates NAFLD via the IL6-SOCS3-SREBP1c signaling pathway and therefore, may represent a promising approach for NAFLD treatment.

HDA-2-Containing Complex Is Required for Activation of Catalase-3 Expression in Neurospora crassa.

It is essential for aerobic organisms to maintain the homeostasis of intracellular reactive oxygen species (ROS) for survival and adaptation to the environment. In line with other eukaryotes, the catalase of Neurospora crassa is an important enzyme for clearing ROS, and its expression is tightly regulated by the growth phase and various oxidative stresses. Our study reveals that, in N. crassa, histone deacetylase 2 (HDA-2) and its catalytic activity positively regulate the expression of the catalase-3 (cat-3) gene. HDA-2, SIF-2, and SNT-1 may form a subcomplex with such a regulation role. As expected, deletion of HDA-2 or SIF-2 subunit increased acetylation levels of histone H4, indicating that loss of HDA-2 complex fails to deacetylate H4 at the cat-3 locus. Furthermore, loss of HDA-2 or its catalytic activity led to dramatic decreases of TFIIB and RNA polymerase II (RNAP II) recruitment at the cat-3 locus and also resulted in high deposition of H2A.Z at the promoter and transcription start site (TSS) regions of the cat-3 gene. Collectively, this study strongly demonstrates that the HDA-2-containing complex activates the transcription of the cat-3 gene by facilitating preinitiation complex (PIC) assembly and antagonizing the inhibition of H2A.Z at the cat-3 locus through H4 acetylation. IMPORTANCE Clearance of reactive oxygen species (ROS) is critical to the survival of aerobic organisms. In the model filamentous fungus Neurospora crassa, catalase-3 (cat-3) expression is activated in response to H2O2-induced ROS stress. We found that histone deacetylase 2 (HDA-2) positively regulates cat-3 transcription in N. crassa; this is widely divergent from the classical repressive role of most histone deacetylases. Like HDA-2, the SIF-2 or SNT-1 subunit of HDA-2-containing complex plays a positive role in cat-3 transcription. Furthermore, we also found that HDA-2-containing complex provides an appropriate chromatin environment to facilitate PIC assembly and to antagonize the inhibition role of H2A.Z at the cat-3 locus through H4 acetylation. Taken together, our results establish a mechanism for how the HDA-2-containing complex regulates transcription of the cat-3 gene in N. crassa.