The results confirm that the circulating levels of miR-21, miR-145, miR-155, and miR-191 are increased in patients with arsenism caused by coal-burning and these miRNAs inhibit the target genes of pathways related to immune inflammation, oxidative stress, and DNA damage repair.

Background: Previous studies have reported controversial results on levels of inflammatory cytokines in patients with arsenic exposure. This study aims to evaluate the associations between arsenic exposure and inflammatory cytokines and C-reaction protein (CRP). Methods: We searched the databases including PubMed, Embase, Web of Science, and China national knowledge infrastructure (CNKI) for studies reporting levels of cytokines and CRP in patients with arsenic exposure compared to the controls. The retrieval time was from January 2000 to September 2022. Results: 13 observational studies involving 1665 arsenic exposed and 1091 unexposed individuals were included. Among these studies, 6 from China, 4 from India, 2 from Bangladesh and 1 from Turkey. Our result showed that interleukin (IL)-6, IL-8, and IL-12 levels were significantly higher in arsenic-exposed individuals compared to the control group, IL-2 level was significantly lower, and Tumor necrosis factor-α, Interferon-γ, CRP, and IL-10 levels were not changed. After sensitivity analyses, tumor necrosis factor-α and Interferon-γ levels were significantly higher in arsenic-exposed individuals compared to the control group. High heterogeneity was detected in most studies. Conclusion: Many cytokines (such as IL-6, IL-8, and IL-12) have altered in individuals with arsenic exposure, this indicates arsenic exposure could trigger the cell-mediated inflammatory response. Regular examining immune function (such as inflammatory cytokines) in individuals with the risk of arsenic exposure is important to human health.

Ar-turmerone, a compound isolated from turmeric seeds, has exhibited anti-malignant, anti-aging and anti-inflammatory properties. Here, we assessed the effects of ar-turmerone on glioma cells. U251, U87 and LN229 glioma cell lines were treated with different concentrations of ar-turmerone (0, 50, 100 and 200 μM), and their viability and mobility were evaluated using Cell Counting Kit 8, colony formation, wound healing and Transwell assays. The effects of ar-turmerone on U251 glioma cell proliferation were also assessed using a subcutaneous implantation tumor model. High-throughput sequencing, bioinformatic analyses and quantitative real-time polymerase chain reactions were used to identify the key signaling pathways and targets of ar-turmerone. Ar-turmerone reduced the proliferation rate and mobility of glioma cells in vitro and arrested cell division at G1/S phase. Cathepsin B was identified as a key target of ar-turmerone in glioma cells. Ar-turmerone treatment reduced cathepsin B expression and inhibited the cleavage of its target protein P27 in glioma cells. On the other hand, cathepsin B overexpression reversed the inhibitory effects of ar-turmerone on glioma cell proliferation, mobility progression in vitro and in vivo. In conclusion, ar-turmerone suppressed cathepsin B expression and P27 cleavage, thereby inhibiting the proliferation and mobility of glioma cells.

The lead-free double-perovskite Cs₂AgBiBr₆, which combines nontoxicity with superior stability, has been highlighted as an ecofriendly alternative to lead-halide perovskites in photoelectric devices by recent advancements. Herein, Cs₂AgBiBr₆ films were successfully synthesized on a fluorine-doped tin oxide (FTO) glass substrate via a spin-coating method in a dry-air glovebox (relative humidity (RH) less than 20%), eliminating the need for antisolvent dripping or inert gas protection. The films exhibited a uniform morphology, with root-mean-square (RMS) and average (R _a) roughness values of 15.4 and 11.9 nm, respectively. The fabricated Cs₂AgBiBr₆-based memristors demonstrated stable, repeatable bipolar resistive switching behavior with low operating voltages (+0.4 V, −0.3 V), an on/off ratio of 479, an endurance of 1000 cycles, and a retention time of 10⁴ s. Remarkably, the resistance ratio between the high-resistance state (HRS) and low-resistance state (LRS) remained stable at approximately 441 even after 30 days of ambient storage. Furthermore, the memristor mimicked biological synaptic functions, achieving an accuracy of 91.39% in machine learning simulations. These findings highlight the viability of using Cs₂AgBiBr₆ in both memory and computational applications, thus offering a promising pathway for developing sustainable and efficient memristor-based systems for use in neuromorphic computing and information storage.

Arsenic is a prevalent environmental pollutant that targets the nervous system of living beings. Recent studies indicated that microglial injury could contribute to neuroinflammation and is associated with neuronal damage. Nevertheless, the neurotoxic mechanism underlying the arsenic-induced microglial injury requires additional research. This study explores whether cathepsin B promotes microglia cell damage caused by NaAsO₂. Through CCK-8 assay and Annexin V-FITC and PI staining, we discovered that NaAsO₂ induced apoptosis in BV2 cells (a microglia cell line). NaAsO₂ was verified to increase mitochondrial membrane permeabilization (MMP) and promote the generation of reactive oxygen species (ROS) through JC-1 staining and DCFDA assay, respectively. Mechanically, NaAsO₂ was indicated to increase the expression of cathepsin B, which could stimulate pro-apoptotic molecule Bid into the activated form, tBid, and increase lysosomal membrane permeabilization by Immunofluorescence and Western blot assessment. Subsequently, apoptotic signaling downstream of increased mitochondrial membrane permeabilization was activated, promoting caspase activation and microglial apoptosis. Cathepsin B inhibitor CA074-Me could mitigate the damage of microglial. In general, we found that NaAsO₂ induced microglia apoptosis and depended on the role of the cathepsin B-mediated lysosomal-mitochondrial apoptosis pathway. Our findings provided new insight into NaAsO₂-induced neurological damage.

In recent years, the influence of environmental factors on organismal aging has garnered increasing attention. Studies have shown that sleep deprivation and environmental pollutants could accelerate the emergence of multiple organismal aging phenotypes. In addition, studies have shown that chronic exposure to sodium arsenite (iAs) induces skeletal muscle atrophy and the inhibition of melatonin secretion in rats. This study aimed to reveal the synergistic effect of sleep deprivation and arsenite exposure on skeletal muscle aging, including reduced limb grip strength and skeletal muscle mass, along with the serum levels of melatonin (MT) and cortisol (COR) in C57BL/6J mice. The results demonstrated that while exposure to arsenite for 12 weeks or sleep deprivation (SD) for 4 weeks did not exert significant effects on limb grip strength or skeletal muscle mass, their combination exhibited a synergistic effect on skeletal muscle aging. Notably, the iAs+SD group exhibited a significant decline in limb grip strength by Week 12, accompanied by a reduced gastrocnemius muscle mass and muscle index. The pathological analysis showed muscle fiber atrophy, a shift towards slow-twitch muscle fibers (type I), and shortened telomere length. Additionally, oxidative damage was increased in the SD and iAs+SD groups, with decreased levels of SOD and GPx and elevated levels of MDA in the iAs+SD group. The serum MT level and MT/COR ratio were significantly reduced, while the serum COR level was elevated in the iAs+SD group compared to the other groups. A correlation analysis further revealed that the serum MT level and the MT/COR ratio were positively correlated with limb grip strength, muscle index, and telomere length, whereas the serum COR level exhibited negative correlations with these parameters. These findings suggest that sleep deprivation and subchronic exposure to arsenite synergistically induce skeletal muscle aging, and that the disruption of the balance between MT and COR potentially serves as a significant risk factor.