Abstract Atherosclerosis accounts for major mortality of cardiac‐cerebral vascular diseases worldwide. Pathologically, persistent inflammation dominates the progression of atherosclerosis, which can be accelerated by a high‐fat diet (HFD), possibly through triggering local intestinal oxidative stress and ensuing gut barrier dysfunction. Current pharmacotherapy has been disappointing, ascribed to limited therapeutic efficacy and undesirable side effects. Hence it is compelling to explore novel efficient anti‐atherosclerotic drugs with minimal toxicity. Herein, two fullerene‐based therapies with exceptional antioxidant capacity, in the form of water‐soluble injectable fullerene nanoparticles (IFNPs) and oral fullerene tablets (OFTs), are demonstrated to retard HFD‐fueled atherosclerosis in ApoE −/‐ mice with favorable biosafety. Especially, OFTs afford robust anti‐atherosclerotic therapeutic even against advanced plaques, besides stabilizing plaques with less lipid deposition and improved collagen expression. Specifically, it is identified that OFTs can ameliorate HFD‐induced dysregulated intestinal redox homeostasis and restore gut barrier integrity, thereby restraining the translocation of luminal lipopolysaccharide (LPS) into the bloodstream. Furthermore, significantly reduced circulating LPS after OFTs treatment contributes to down‐regulated LPS/TLR4/NF‐ κ B signaling in aortic focal, which further mitigates local inflammation and disease development. Overall, this study confirms the universal anti‐atherosclerotic effect of fullerenes and provides a novel therapeutic mechanism via modulating intestinal barrier to attenuate atherosclerosis.
Aquaporins (AQPs) are a subgroup of small transmembrane transporters that are distributed in various types of tissues, including the lung, kidney, heart and central nervous system. It is evident that respiratory diseases represent a significant global health concern, with a considerable number of deaths occurring worldwide. Recent researches have demonstrated that AQPs play a pivotal role in respiratory diseases, including chronic obstructive pulmonary disease (COPD), asthma, acute respiratory distress syndrome (ARDS), and particularly non-small cell lung cancer (NSCLC). In the context of NSCLC, the overexpression of AQP1, AQP3, AQP4, and AQP5 has been demonstrated to facilitate tumor angiogenesis, as well as the proliferation, migration, and invasiveness of tumor cells. This review concisely explores the role of AQP family on respiratory diseases, to assess their clinical and translational significance for understanding molecular pathogenesis. However, the potential translation of AQPs biomarkers into clinical applications is promising and the understanding of the precise mechanisms influencing respiratory diseases is still ongoing. Addressing the challenges and outlining the future perspectives in AQPs development is essential for clinical progress in a concise manner.
Water microdroplets have been demonstrated to exhibit extraordinary chemical behaviors, including the abilities to accelerate chemical reactions by several orders of magnitude and to trigger reactions that cannot occur in bulk water. One of the most striking examples is the spontaneous generation of hydroxyl radical from hydroxide ions. Alcohols and alkoxide ions, being structurally similar to water and hydroxide ions, might exhibit similar behavior on microdroplets. Here, we report the spontaneous generation of alkoxide radicals from alcohols (RCH
Background: Pulmonary small airway epithelia are the primary site of cellular and histological alterations in chronic obstructive pulmonary disease (COPD), while the potential therapeutic hub genes of pulmonary epithelia are rarely identified to elucidate profound alterations in the progression of the disease.Methods: Microarray dataset of GSE11906 containing small airway epithelia from 34 healthy non-smokers and 33 COPD patients was applied to screen differentially expressed genes (DEGs).Weighted gene correlation network analysis (WGCNA) was further used to identify the hub genes related to clinical features.Moreover, single-cell RNA sequencing data from GSE173896 and GSE167295 dataset were applied to explore the expression and distribution of the hub genes.The expression levels of hub genes in epithelial cells stimulated by cigarette smoke extract (CSE) were detected by RT-qPCR.Results: Ninety-eight DEGs correlated with clinical features of COPD were identified via limma and WGCNA.Eight hub genes (including AKR1C3, ALDH3A1, AKR1C1, CYP1A1, GPX2, CBR3, AKR1B1 and GSR) that might exert an antioxidant role in COPD process were identified.Single-cell transcriptomic analysis indicated that the expressions of AKRAC3, ALDH3A1, GPX2, CBR3 and AKR1B1 were significantly increased in the COPD group when compared with the normal group.Moreover, we found that the expression of ALDH3A1 was the most abundantly expressed in ciliated cells.RT-qPCR results indicated that the majority of candidate novel genes were significantly elevated when the epithelial cells were exposed to CSE.Conclusion: Through integrating limma, WGCNA, and protein-protein interaction (PPI) analysis, a total of eight candidate hub genes of pulmonary airway epithelia were identified in COPD.Moreover, single-cell transcriptomic analysis indicated that ALDH3A1 was enriched in ciliated cells, which may provide a new insight into the pathogenesis and treatment of COPD.
The multiphase oxidation of SO2 to sulfate in aerosol particles is a key process in atmospheric chemistry. However, there is a large gap between the observed and simulated sulfate concentrations during severe haze events. To fill in the gaps in understanding SO2 oxidation chemistry, a combination of experiments and theoretical calculations provided evidence for the direct, spin-forbidden excitation of SO2 to its triplet states using UVA photons at an air-water interface, followed by reactions with water and O2 that facilitate the rapid formation of sulfate. The estimated reaction energy for the whole process, 3SO2 + H2O + 1/2O2 → HSO4- + H+ (298 K, 1 M), was ΔGr = -107.8 kcal·mol-1. Moreover, calculations revealed that this was a multistep reaction involving submerged, small energy barriers (∼10 kcal·mol-1). These results indicate that photochemical oxidation of SO2 at the air-water interface with solar actinic light may be an important unaccounted source of sulfate aerosols under polluted haze conditions.
In this work, a magnetic molecularly imprinted polymer (Fe3O4@SiO2@MIPs) was prepared via a surface-imprinted method for the determination of the triazines in environmental water samples combined with high-performance liquid chromatography tandem mass spectrometry (HPLC-MS/MS). The Fourier transform infrared spectroscopy (FTIR) and vibrating sample magnetometer showed that the Fe3O4@SiO2@MIPs was successfully synthesised and exhibited superparamagnetism. The isotherm adsorption, selectivity and adsorption kinetics experiments showed that the Fe3O4@SiO2@MIPs exhibited excellent specific recognition and fast adsorption equilibrium for triazines. The adsorption process is spontaneous and endothermic. The isotherm adsorption was consistent with Scatchard model and adsorption kinetic fit pseudo-second-order kinetic model. Under the optimised adsorption conditions, the Fe3O4@SiO2@MIPs was directly used to selectively enrich six triazines in environmental water samples. The enrichment volume was up to 500 mL, and the matrix effects were down to 0.7–12.4%. The built method has excellent linearities in the range of 0.25–500 ng L−1 with R2 in the range of 0.998–0.999, lower limit of detections (0.02–0.08 ng L−1) and higher precision (2.4–7.2%). The Fe3O4@SiO2@MIPs is expected to be widely applied to the direct enrichment of triazines in bulk environmental water samples.
The unbalanced immune state is the dominant feature of myocardial injury. However, the complicated pathology of cardiovascular diseases and the unique structure of cardiac tissue lead to challenges for effective immunoregulation therapy. Here, we exploited oral fullerene nanoscavenger (OFNS) to maintain intestinal redox homeostasis to resolve systemic inflammation for effectively preventing distal myocardial injury through bidirectional communication along the heart–gut immune axis. Observably, OFNS regulated redox microenvironment to repair cellular injury and reduce inflammation in vitro. Subsequently, OFNS prevented myocardial injury by regulating intestinal redox homeostasis and recovering epithelium barrier integrity in vivo. Based on the profiles of transcriptomics and proteomics, we demonstrated that OFNS balanced intestinal and systemic immune homeostasis for remote cardioprotection. Of note, we applied this principle to intervene myocardial infarction in mice and mini-pigs. These findings highlight that locally addressing intestinal redox to inhibit systemic inflammation could be a potent strategy for resolving remote tissue injury.
Microdroplet chemistry has been an emerging new field for its large plethora of unique properties, among which an especially intriguing one is the strong oxidizing and reducing powers. The hydroxide ion in water microdroplets is considered to split into a hydroxyl radical and an electron at the air-water interface, and the former is responsible for the oxidizing capability while the latter is responsible for the reducing power, making a unity of opposites. However, to date there are only two examples showing that oxidation and reduction occur simultaneously to the same substrates, which might be a result of the redox properties of the substrate per se. In this study, we carefully chose a group of ο-quinone compounds as the substrates in water microdroplets and discovered that they can be both oxidized by the hydroxyl radical and reduced by the electron. These results keep pushing the limit of the unique redox properties of microdroplet chemistry.
'/%3e%3cuse xlink:href='%23a' transform='rotate(23.036 .093 25.536)'/%3e%3cuse xlink:href='%23a' transform='rotate(45.87 1.273 16.18)'/%3e%3cuse xlink:href='%23a' transform='rotate(69.945 .996 12.078)'/%3e%3cuse xlink:href='%23a' transform='rotate(20.66 -19.689 31.932)'/%3e%3c/svg%3e)