Exosomes are nanosized vesicles that have been found to be involved in many diseases. Exosomes can mediate communication between cells in a variety of ways. Certain types of mediators derived from cancer cells can play a crucial role in the development of this pathology, promoting tumor growth, invasion, metastasis, angiogenesis, and immunomodulation. Exosomes in the bloodstream show promise as a future tool for detecting cancer at an early stage. The sensitivity and specificity of clinical exosome biomarkers need to be enhanced. Knowledge of exosomes is not only important for understanding the significance of cancer progression but also for providing clinicians with useful information for the diagnosis, treatment, and discovery of methods to prevent cancer from recurring. The widespread adoption of diagnostic tools based on exosomes may revolutionize cancer diagnosis and treatment. Tumor metastasis, chemoresistance, and immunity are all aided by exosomes. A potential new approach to cancer therapy involves preventing metastasis by inhibiting miRNA intracellular signaling and blocking the formation of pre-metastatic niches. For colorectal patients, exosomes represent a promising area of investigation for improving the diagnosis, treatment, and management. Reported data demonstrate that the serum expression level of certain exosomal miRNA is significantly higher in primary colorectal cancer patients. The present review discusses mechanisms and clinical implications of exosomes in colorectal cancer.

Vesicoureteral reflux (VUR) is one of the most important disorders encountered in pediatric nephrology due to its frequency and potential evolution to chronic kidney disease (CKD). The aim of our study was to identify noninvasive and easy-to-determine urinary markers to facilitate the diagnosis and staging of VUR. We performed a cross-section study including 39 patients with VUR followed over three years (August 2021–September 2023) and 39 children without urinary disorder (the control group). We measured the urinary concentration of interleukin-6 (IL-6), cathelicidin (LL-37), and neutrophil gelatinase-associated lipocalin (NGAL) in VUR and healthy controls. Moreover, we analyzed the correlation between these biomarkers and the presence of renal scars (RS), reflux nephropathy (RN), and CKD. The NGAL concentrations were significantly higher in patients with VUR than in the controls (p = 0.02). Regarding the severity of the reflux, NGAL/creatinine and LL-37/creatinine were positively correlated with severe reflux (p = 0.04, respectively, p = 0.02). In patients with VUR and RS, LL-37/creatinine was significantly lower (p = 0.01). LL-37/creatinine with an AUC of 0.71 and NGAL/creatinine with an AUC of 0.72 could be acceptable diagnostic tests for severe VUR. In conclusion, urinary IL-6, NGAL, and LL-37 could serve as valuable markers for diagnosing and predicting outcomes in patients with VUR and RN.

Liver fibrosis can develop after sustained oxidative stress and inflammatory signaling and transforming growth factor-β (TGF-β) is a key profibrotic mediator. Rutin (Ru) is a plant-derived flavonoid with antioxidant and anti-inflammatory effects, but with limited bioavailability, which impedes therapeutic efficacy. This study investigated the hepatoprotective potential of rutin-phytoreduced gold nanoparticles (RuAuNPs) in a thioacetamide (TAA)-induced rat model of liver fibrosis. RuAuNPs were spherical, 18nm diameter (transmission electron microscopy -TEM) and exhibited SPR peak at 523nm (UV–Vis spectroscopy). Following liver fibrosis induction, animals were treated with free rutin or RuAuNPs. Oxidative stress (spectrophotometry, fluorimetry), inflammation (ELISA) and liver morphology (histopathology, TEM) were evaluated. TAA induced hepatic injury and fibrotic remodeling, associated with elevated TGF-β expression, oxidative stress, and inflammation. Free rutin showed limited recovery of liver parameters. RuAuNP treatment significantly improved hepatic histology and ultrastructure, reduced TGF-β and pro-inflammatory cytokine levels (TNFα, IL1β, IL6), decreased oxidative stress damage (lipid peroxidation), restored glutathione redox balance, and enhanced superoxide dismutase activity. Improvement in the AST/ALT ratio suggested early functional recovery, despite persistent aminotransferase elevation. Overall, RuAuNPs enhanced rutin’s antifibrotic and hepatoprotective effects by targeting oxidative and inflammatory pathways and can represent an effective delivery system for rutin in liver fibrosis therapy.

Liver fibrosis is driven by persistent oxidative stress and inflammatory signaling, with transforming growth factor-β (TGF-β) acting as a key profibrotic mediator. Rutin (Ru) is a plant-derived flavonoid with antioxidant and anti-inflammatory effects, but its low bioavailability limits therapeutic efficacy. This study investigated whether rutin-phytoreduced gold nanoparticles (RuAuNPs) enhanced rutin delivery leading to antifibrotic and anti-inflammatory effects in a rat model of liver fibrosis. Liver fibrosis was induced by oral administration of thioacetamide (TAA, 150 mg/kg body weight, p.o.) for six weeks. Following fibrosis induction, the animals were treated with free rutin (30 mg/kg body weight), RuAuNPs (0.3 mg/kg body weight), or AuNPs (0.3 mg/kg body weight), both expressed as nanoparticle mass, all administered orally for four weeks. RuAuNPs were synthesized by green rutin-mediated reduction and further characterized by TEM, DLS, and FTIR spectroscopy; they were spherical, showing an average hydrodynamic size of 104.1 nm (PDI 0.345). FTIR confirmed rutin capping. Biological effects were evaluated by liver morphology (H&E histology, TEM), biochemical assessment of liver aminotransferases and glico-lipidic status, ELISA and spectrophotometry measurement of redox biomarkers (lipid peroxidation, glutathione status, antioxidant enzymes), cytokines (TNF-α, IL-1β, IL-6), and TGF-β. TAA-induced hepatic injury and remodeling with increased profibrotic signaling, oxidative stress, and inflammation. Free rutin slightly ameliorated the liver damage, whereas RuAuNP improved histological features, reduced TGF-β and pro-inflammatory cytokines, decreased lipid peroxidation, and supported antioxidant defenses. Overall, RuAuNP may enhance rutin efficacy in TAA-induced liver fibrosis, with novelty stemming from the integrated in vivo evaluation of tissue changes and key profibrotic/oxidative/inflammatory pathway.

Supplement use has increased in recent years, despite limited evidence for its broad health benefits. Furthermore, exogenous antioxidants may determine pro-oxidant effects, depending on various factors such as dose, circadian window, and presence of metal ions. Although the effects of sleep deprivation (SD) on the brain are well-documented, its impact on peripheral organs remains relatively underexplored. The goal of this study was to evaluate the effects of a Cornus mas (C. mas) fruit extract on multiple peripheral sites in rats undergoing paradoxical sleep deprivation (PSD). Male Wistar rats were randomly distributed in four groups, including control, C. mas (CM), sleep deprivation (SD), and sleep deprivation and C. mas (SD+CM) (n = 7/group). Seven days of PSD were associated with ultrastructural liver injury and evidence of oxidative dysfunction in several organs: liver, kidney, spleen, and aorta. These alterations were accompanied by marked increases in the evaluated cytokines, including testicular Interleukin-1β, hepatic Interleukin-6, and aortic Interleukin-4. Although the C. mas extract largely maintained hepatic ultrastructure, its effects on other organs were limited. In the aorta, it normalized GSSG values but was also associated with a significant increase in lipid peroxidation. These findings highlight both the systemic impact of SD and caution against assuming uniform benefits of exogenous antioxidants across organ systems in this context.