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Cancer is now the second leading cause of death after cardiovascular diseases. Although there are many different cancer treatments available, all of them have serious side effects and drug resistance. Therefore, scientists are searching for natural products that can effectively prevent the occurrence of cancers. Studies have shown that the consumption of citrus fruits can reduce the risk of several diseases, including cancers, and its anti-cancer effects are attributed to a variety of bioactive ingredients. This article systematically summarizes recent progress in research on the major anti-cancer ingredients in citrus fruits and their molecular mechanisms. Citrus is one of the important fruits with high medicinal value. In-depth studies on its anti-cancer effects and molecular mechanisms will help to enhance its industrial value, and provide a theoretical basis for the processing and development of citrus fruits into functional foods for chemical prevention of cancers. As the anti-cancer constituents and mechanisms of citrus fruits have been understood fully, their application as a natural source of anti-cancer agents in clinical cancer treatments can be expected soon.

Twenty-two coumarins and twenty-six flavonoids were quantitated in fingered citron in different growth periods. Limettin was the top coumarin, and diosmin was the highest flavonoid, followed by hesperidin. Antioxidant evaluation by DPPH, ABTS, and FRAP indicated extracts of fingered citron in three growth periods all showed good antioxidant activity, which was positively correlated with the concentration of extracts. The oxidative stress model of RAW264.7 cells indicated extracts from fingered citron effectively reduced the contents of NO, MDA, and ROS in cells and increased the activity of SOD, thereby alleviating cell damage. The antioxidant capacity of fingered citron in November was the highest, followed by July and September. And there was a significantly positive correlation between the total flavonoid content and the antioxidant capacity. Diosmin, hesperidin, and neohesperidin were the main contributors to antioxidation. This study has significance for utilization of fingered citron germplasm resources and development of related functional products. [ABSTRACT FROM AUTHOR]

This study addresses the critical issue of traffic safety in winter, particularly focusing on the challenges posed by ice and snow on roads. Traditional methods of snow and ice removal are often labor-intensive, inefficient, and environmentally harmful. The objective is to develop a more effective solution for asphalt pavement deicing. Inspired by the anti-icing coating technology used in high-voltage conductors, this research develops an ice-suppressing material designed to reduce the adhesion between snow, ice, and pavement surfaces. The material's performance is evaluated in terms of deicing efficiency, durability, adhesive properties, and its impact on pavement performance. Test results demonstrate that the developed ice-suppressing material significantly reduces the adhesion between the ice layer and the pavement, facilitating easier removal. This study concludes that the developed ice-suppressing material significantly enhances deicing efficiency on asphalt pavements. It exhibits strong hydrophobic properties, as evidenced by increased water droplet contact angles on coated surfaces (99.5° to 83.3°) compared to clean glass slides (39.2° to 29°). This hydrophobicity effectively reduces ice adhesion, decreasing tensile and shear strength of the ice layer by 38.2% and 63.6%, respectively. Additionally, the material demonstrates superior ice-melting capabilities in sub-zero temperatures, with coated ice cubes showing a higher mass reduction rate than uncoated ones. Importantly, its slow-release nature ensures sustained deicing performance over multiple cycles, maintaining effectiveness after seven test cycles. This study introduces an innovative ice-suppressing material that not only improves the efficiency and environmental impact of deicing methods but also contributes to enhancing road safety in winter conditions. The material's novel composition and sustained effectiveness present a significant advancement in the field of winter road maintenance. [ABSTRACT FROM AUTHOR]

Background: Pulmonary hypertension (PH) is a rare and fatal disease, the pathological changes of which include pulmonary arterial smooth muscle cell (PASMC) proliferation, which is the pathological basis of pulmonary vascular remodeling. Studies have demonstrated that chromatin-associated circRNA can regulate a variety of biological processes, including PASMC proliferation in patients with hypoxic PH. However, the role of chromatin-associated circRNA in the proliferation of PH remains largely unexplored. In this study, we aimed to identify the function and mechanism of chromatin-associated circRNA in PASMC proliferation in PH., Methods: The role of ca-circFOXP1 was investigated in hypoxic mouse PASMCs and SuHX (Sugen5416+hypoxia) model mice through the use of antisense oligonucleotide knockdown and adeno-associated virus-mediated knockdown. Through bioinformatic sequence alignment, chromatin isolation by RNA purification, Cell Counting Kit 8, 5-ethynyl-2-deoxyuridine, Western blot, and other experiments, the function and mechanism of ca-circFOXP1 were verified., Results: The expression of ca-circFOXP1 was found to be significantly increased in SuHX model mice and hypoxic mouse PASMCs. Moreover, ca-circFOXP1 was found to regulate the level of the host protein FOXP1 (forkhead box protein 1) through the R loop, thereby influencing the phosphorylation activity of SMAD2 (SMAD family member 2) and, consequently, the proliferation of mouse PASMCs. It is noteworthy that the m6A modification was found to promote the formation of the R loop between ca-circFOXP1 and the host gene FOXP1 , thereby regulating the expression of the host protein. Furthermore, we have identified that the splicing factor SRSF4 (serine/arginine rich splicing factor 4) can upregulate the expression of ca-circFOXP1 by splicing exons 6 and 9 of FOXP1 pre-mRNA., Conclusions: The results demonstrated that the splicing factor SRSF4 upregulated the expression of ca-circFOXP1, and m6A methylation promoted R-loop formation between ca-circFOXP1 and host genes, regulated the level of host protein FOXP1, and then affected the phosphorylation activity of SMAD2, mediating PASMC proliferation, leading to pulmonary vascular remodeling. These results provide a theoretical basis for further study of the pathological mechanisms of hypoxic PH and may provide certain insights.

Background: Pulmonary hypertension is a rare, progressive disorder that can lead to right ventricular hypertrophy, right heart failure, and even sudden death. N6-methyladenosine modification and the main methyltransferase that mediates it, methyltransferase-like (METTL) 3, exert important effects on many biological and pathophysiological processes. However, the role of METTL3 in pyroptosis remains unclear., Methods and Results: Here, we characterized the role of METTL3 and the underlying cellular and molecular mechanisms of pyroptosis, which is involved in pulmonary hypertension. METTL3 was downregulated in a pulmonary hypertension mouse model and in hypoxia-exposed pulmonary artery smooth muscle cell. The small interfering RNA-induced silencing of METTL3 decreased the m6A methylation levels and promoted pulmonary artery smooth muscle cell pyroptosis, mimicking the effects of hypoxia. In contrast, overexpression of METTL3 suppressed hypoxia-induced pulmonary artery smooth muscle cell pyroptosis. Mechanistically, we identified the phosphate and tension homology deleted on chromosome 10 (PTEN) gene as a target of METTL3-mediated m6A modification, and methylated phosphate and tension homology deleted on chromosome 10 mRNA was subsequently recognized by the m6A "reader" protein insulin-like growth factor 2 mRNA-binding protein 2, which directly bound to the m6A site on phosphate and tension homology deleted on chromosome 10 mRNA and enhanced its stability., Conclusions: These results identify a new signaling pathway, the METTL3/phosphate and tension homology deleted on chromosome 10/insulin-like growth factor 2 mRNA-binding protein 2 axis, that participates in the regulation of hypoxia-induced pyroptosis.