The aim of the present study was to determine the roles of the chemotactic factor, chemokine ligand 2 (CCL2), and its receptor, chemokine receptor type 2 (CCR2), in the hippocampus of rats with cerebral ischemia/reperfusion injury. In total, 24 Sprague‑Dawley rats, weighting 250‑300 g, were randomly divided into three groups (n=8): Sham‑operated (C group), cerebral ischemia/reperfusion injury (I/R group) and propofol‑intervention (P group) groups. The rats were sacrificed at 6 h after the ischemia/reperfusion surgery, and the brains were obtained to isolate the hippocampus. The mRNA expression levels of CCL2 and CCR2 in the hippocampus were analyzed by quantitative polymerase chain reaction, while the protein expression levels of CCL2 and CCR2 were determined by western blot analysis. The expression levels of CCL2 and CCR2 in the procerebrum were markedly elevated in the I/R and P groups at 6 h after the ischemia/reperfusion surgery when compared with the C group (P<0.05). In addition, the mRNA expression levels of CCL2 and CCR2 decreased significantly in the P group as compared with that in the I/R group (P<0.05). Therefore, CCL2 and CCR2 may be involved in the mechanisms underlying cerebral ischemia/reperfusion injury, and propofol may protect the brain through regulating the expression of CCL2 and CCR2.

Perfluorooctanoic acid (PFOA) is a globally pervasive environmental contaminant characterized by chemical stability and bioaccumulation through the food chain, posing serious health risks to both humans and animals. Accumulating evidence has linked PFOA exposure to the development of various cancers, including prostate cancer (PCa), renal cancer, breast cancer, and ovarian cancer. However, the molecular mechanisms by which PFOA promotes PCa progression remain unclear. In this study, we demonstrate that low-dose PFOA exposure enhances the expression of mitogen-activated protein kinase 15 (MAPK15), thereby promoting autophagy and facilitating tumor cell proliferation. Mechanistically, PFOA binds to the N6-methyladenosine (m⁶A) demethylase FTO (fat mass and obesity-associated protein), inhibiting its demethylase activity and resulting in elevated m⁶A modification levels on MAPK15 mRNA. This modification leads to increased MAPK15 protein expression, which in turn activates autophagy pathways and drives the proliferation, migration, and invasion of PCa cell lines. Collectively, our findings provide critical molecular evidence for the carcinogenic potential of PFAS compounds and offer new insights into environmental toxicology and ecological risk assessment.

Perfluorooctanoic acid (PFOA), a persistent organic pollutant known for its chemical stability, is widely dispersed in the environment, posing significant health risks to mammals through various exposure routes such as ingestion, inhalation, and dermal contact. In this study, mice were exposed to PFOA (0, 0.2, 2 mg/L) through drinking water for 180 days to investigate its toxic effects on the colon. We identified differentially expressed genes through RNA sequencing and validated the impact of PFOA on the expression of these genes in colon tissue. Our findings revealed that long-term exposure to PFOA caused inflammatory bowel disease (IBD)-like damage to the mouse colon. We found PFOA could induce damage to the intestinal barrier. Inhibition of the Wnt signaling pathway following PFOA exposure results in impaired stem cell function in the colon of mice. Furthermore, PFOA activated the PPAR signaling pathway, disrupting cellular lipid metabolism in colon tissues. Additionally, PFOA induced inflammatory responses in colon tissue, facilitating NLR family, pyrin domain containing 3 (NLRP3) inflammasome activation and cell apoptosis. This study offers a thorough understanding of the mechanisms responsible for the damage to mouse colon tissue resulting from long-term exposure to PFOA.

The properties of nanopipettes largely rely on the materials introduced onto their inner walls, which allow for a vast extension of their sensing capabilities. The challenge of simultaneously enhancing the sensitivity and selectivity of nanopipettes for pH sensing remains, hindering their practical applications. Herein, we report insulin-modified nanopipettes with excellent pH response performances, which were prepared by introducing insulin onto their inner walls via a two-step reaction involving silanization and amidation. The pH response intensity based on ion current rectification was significantly enhanced by approximately 4.29 times when utilizing insulin-modified nanopipettes compared with bare ones, demonstrating a linear response within the pH range of 2.50 to 7.80. In addition, insulin-modified nanopipettes featured good reversibility and selectivity. The modification processes were monitored using the I-V curves, and the relevant mechanisms were discussed. The effects of solution pH and insulin concentration on the modification results were investigated to achieve optimal insulin introduction. This study showed that the pH response behavior of nanopipettes can be greatly improved by introducing versatile molecules onto the inner walls, thereby contributing to the development and utilization of pH-responsive nanopipettes.

Human mesenchymal stem cells (hMSCs) possess broad prospects in pre-clinical research. In vitro amplification requires appropriate medium to reach the number of seed cells with clinical significance. However, the uncertainty of the heterologous components of the traditional fetal bovine serum (FBS) culture medium has great safety risks. Then existing commercial hMSCs medium is very expensive, a safer and more economical hMSCs medium is urgently needed. Therefore, we developed a noval hMSCs medium without xenogenic components, it is mainly composed of knockout serum replacement (KSR), constituting additionally four components such as fibroblast growth factor and transferrin, named E5 SFM. Here, we mainly compared the E5 SFM with traditional FBS-containing medium and a commercial medium by surface markers testing, proliferation assay, adipogenic and osteogenic differentiation assessment. We demonstrated that hMSCs cultured in the E5 SFM showed similar morphological characteristics and immunophenotypes to those in other media. Notably, cell proliferative capability was similar to that in the commercial medium, but higher than that in the FBS-containing medium and other media, their capabilities of adipogenic and osteogenic differentiation was significantly higher than other media. Consequently, we concluded that the E5 SFM medium can not only effectively promote cell proliferation of hMSCs, but also has low price and clear and simple ingredients.