Chlamydia trachomatis (Ct) can induce scarring disease of the ocular mucosa, known as trachoma, the most common infectious cause of blindness worldwide. We hypothesized that epithelial-mesenchymal transition (EMT) contributes to the fibrotic process in trachomatous scarring. Infection of human conjunctival epithelial cells (HCjE) with Ct activated signaling pathways involved in EMT induction, which was correlated with decreased expression of E-cadherin, guardian of the epithelial phenotype. In addition, Ct infection was associated with increased expression of two mesenchymal cell markers: fibronectin and α-SMA. The DNA methylation statuses of selected regions of E-cadherin, fibronectin, and α-SMA genes revealed that Ct infection was accompanied with changes in DNA methylation of the E-cadherin promoter, while the expression of the two mesenchymal markers was not related with this epigenetic event. Our data suggest that Ct infection of conjunctival epithelial cells induces EMT-like changes that go along with modification of the methylation profile of the E-cadherin promoter and could, as one of the earliest events, contribute to processes triggering conjunctival scarring.

Diabetic foot ulcers have an enormous impact on patients’ quality of life and represent a major economic burden. The cause is delayed and incomplete wound healing due to hyperglycemia, reduced blood flow, infections, oxidative stress and chronic inflammation. Plasma-activated water (PAW) is emerging as a new therapeutic approach in wound treatment, as it has many of the advantages of cold atmospheric plasma but is easier to apply, thus allowing for widespread use. The aim of this study was to investigate the potential of PAW to improve wound healing in diabetic rats, with a focus on uncovering the underlying mechanisms. Two full-thickness wounds in control and diabetic animals were treated with PAW, and healing was monitored for 15 days at five time points. PAW improved wound healing in diabetic rats and mainly affected the inflammatory phase of wound healing. Application of PAW decreased the number of inflammatory cells, myeloperoxidase (MPO) and N-acetyl-b-D-glycosaminidase (NAG) activity, as well as the mRNA expression of proinflammatory genes in diabetic rats. Ten days after injury, PAW treatment increased collagen deposition in the diabetic animals by almost 10% without affecting collagen mRNA expression, and this is in correlation with a decrease in the Mmp-9/Timp-1 ratio. In conclusion, PAW treatment affects wound healing by reducing the inflammatory response and influencing extracellular matrix turnover, suggesting that it has great potential to accelerate the healing of diabetic wounds.

Silibinin has considerable therapeutic potential for the treatment of diabetes through anti-inflammatory, antioxidant, and immunomodulatory properties. However, the therapeutic application of silibinin is quite limited due to its poor bioavailability. In the present study, an attempt was made to improve the antidiabetic efficacy of silibinin by its encapsulation in liposomal vesicles. The liposomes with a high encapsulation efficiency of silibinin (96%) and a zeta potential of −26.2 ± 0.6 mV were developed and studied using nicotinamide/streptozotocin-induced diabetic rats. Administration of silibinin-loaded liposomes to diabetic rats lowered glucose levels, increased insulin levels, and improved pancreatic islet architecture. The anti-inflammatory effect of silibinin-loaded liposomes was demonstrated by a decrease in serum C-reactive protein (CRP) levels and a reduced deposition of collagen fibers in the islets of diabetic rats. Furthermore, silibinin-loaded liposomes were more efficient in lowering glucose, alanine transaminase, triglyceride, and creatinine levels in diabetic rats than pure silibinin. In addition, silibinin-loaded liposomes had a significantly better effect on beta-cell mass and Glut2 glucose receptor distribution in diabetic islets than pure silibinin. The present results clearly show that liposome encapsulation of silibinin enhances its antidiabetic efficacy, which may contribute to the therapeutic benefit of silibinin in the treatment of diabetes and its complications.