Objective: In this study, β-cyclodextrin (β-CD) was chosen as the coating for ellagic acid to prepare ellagic acid microspheres, and the effect of microspheres on the growth of HepG2 cells was observed. Methods: Scanning electron microscopy, infrared spectroscopy, and release rate analysis were used to identify the formation of ellagic acid microspheres. Methyl thiazolyl tetrazolium (MTT) assay was used to detect the effect of different concentrations of ellagic acid microspheres on tumor cell proliferation at 6, 12, 24 and 36 h, and cell morphology and quantity were observed using hematoxylin-eosin (HE) staining. Single-cell gel electrophoresis was used to observe the effect of ellagic acid microspheres on the DNA damage of HepG2 cells, and the Olive tail moment and the mRNA expression of tumor suppressor protein gene p53 was measured. Results: β-CD could be used as wrapping material of ellagic acid to prepare ellagic acid microspheres. HepG2 cell proliferation could be inhibited by 0.1, 0.3 and 0.5 g/L of ellagic acid microspheres in a dose- and time-dependent manner, and the mechanism of proliferation inhibition was related to DNA damage and cell apoptosis. Conclusion: Preparing ellagic acid microspheres with β-CD is feasible, and ellagic acid microspheres have potential therapeutic value (anticancer).

Microplastics and antibiotic resistance genes are two new pollutants in water environments, and they have potential risks to human health and ecological safety. On the basis of the accumulation of pollutants and microorganisms in sediment, macrobenthic invertebrates are considered as potential practitioners of microplastic degradation and antibiotic resistance gene (ARG) transfer. However, whether microplastic degradation can affect ARG transfer in aquatic environments, especially in the gut of macrobenthic invertebrates, remains unclear. In this study, we demonstrated that microplastics including polyethylene terephthalate (PET), polyvinyl chloride(PVC), polyamide (PA), polystyrene (PS), polypropylene (PP), polyethylene (PE), and polyurethane (PU), and ARGs including tetA, sul1, sul2, and sul3 were widely distributed in sediment and benthic invertebrates in Nansi lake. The distribution of ARGs was related to the number and size of microplastic particles. In particular, it was found for the first time that the content of ARGs corresponding to individual particles was linearly and negatively correlated with the size of microplastics. The results of animal feeding experiments showed that microplastic degradation in the gut of Chironomidae larvae could promote the conjugative transfer of ARGs. The underlying molecular mechanism was SOS response. This study provides a new method for the analysis of the interaction effect of multiple pollutants in freshwater environments.

The cyclic guanosine monophosphate-adenosine monophosphate synthase–stimulator of interferon genes (cGAS–STING) pathway is a cornerstone of host innate immunity, playing a central role in detecting cytosolic double-stranded DNA of both endogenous and exogenous origins. Upon activation, cGAS synthesizes the second messenger 2′3′-cyclic GMP-AMP (cGAMP), which binds and activates STING to trigger downstream immune responses, including the production of type I interferons and proinflammatory cytokines. Emerging studies highlight the cGAS–STING pathway as a promising therapeutic target for preventing and treating diverse pathologies, with particularly transformative potential in anticancer therapies. In this review, we dissect the key findings, functions, and associated components of the cGAS–STING pathway. In addition, we emphasize the factors that upregulate or downregulate the pathway, as well as the role of the cGAS–STING pathway in health and disease. By integrating mechanistic insights with clinical perspectives, this review aims to bridge fundamental discoveries with therapeutic applications of cGAS–STING biology.

Objective: In order to overcome the insolution and low bioavailability of the vitexin in vivo, β-cyclodextrin-vitexin (β-CD–vitexin) microspheres were prepared, and their effects on the proliferation of SW480 cells were observed. Methods: Scanning electron microscopy, ultraviolet spectrum, Fourier transform infrared spectroscopy, and release rate analysis were used to identify the formation of β-CD–vitexin microspheres. MTT assay was used to detect the effect of β-CD–vitexin microspheres on tumor cell proliferation at 6, 12, 24, and 48 h. Fluorescence microscopy and flow cytometry were used to observe the effect of β-CD–vitexin microspheres on the apoptosis of SW480 cells. The mRNA expression of p53 gene was measured by qPCR. Results: β-CD–vitexin microspheres were successfully prepared. SW480 cell proliferation was inhibited by 0.1, 0.2, and 0.4 mg/mL of β-CD–vitexin microspheres in a dose- and time-dependent manner, and the mechanism of proliferation inhibition was related to cell apoptosis caused by the upregulated expression of p53 gene. Conclusion: The preparation of β-CD–vitexin sustained release microspheres is feasible, and β-CD–vitexin microspheres have potential anti-colorectal cancer value.