Acute wounds do not generally require professional treatment modalities and heal in a predictable fashion, but chronic wounds are mainly accompanied with infection and prolonged inflammation, leading to healing impairments and continuous tissue degradation. Although a vast amount of products have been introduced in the market, claiming to provide a better optimization of local and systemic conditions of patients, they do not meet the expectations due to being expensive and not easily accessible, requiring wound care facilities, having patient-specific response, low efficiency, and severe side-effects. In this sense, developing new, safe, self-applicable, effective, and cheap wound care products with broad-range antimicrobial activity is still an attractive area of international research. In the present work, boron derivatives [boric acid and sodium pentaborate pentahydrate (NaB)] were evaluated for their antimicrobial activity, proliferation, migratory, angiogenesis, gene, and growth factor expression promoting effects on dermal cells in vitro. In addition, boron-containing hydrogel formulation was examined for its wound healing promoting potential using full-thickness wound model in streptozotocin-induced diabetic rats. The results revealed that while both boron compounds significantly increased proliferation, migration, vital growth factor, and gene expression levels of dermal cells along with displaying remarkable antimicrobial effects against bacteria, yeast, and fungi, NaB displayed greater antimicrobial properties as well as gene and growth factor expression inductive effects. Animal studies proved that NaB-containing gel formulation enhanced wound healing rate of diabetic animals and histopathological scores. Overall data suggest a potential promising therapeutic option for the management of chronic wounds but further studies are highly warranted to determine signaling pathways and target metabolisms in which boron is involved to elucidate the limitations and extend its use in clinics.

Cisplatin (CP) is one of the most preferred platinum-containing antineoplastic drugs. However, even in nontoxic plasma concentrations, it may cause kidney injury. To be able to increase its effective pharmacological dose, its side effects need to be regarded. Diet restriction (DR) has been demonstrated to improve cellular survival in a number of disorders. In this context, we investigated the role of DR in CP-induced nephrotoxicity (CPN). Besides alternate DR, animals were exposed to DR for 3 days prior or after CP treatment. Here, we observed that both 3 days of DR reverses the nephrotoxic effect of CP, which was associated with improved physiological outcomes, such as serum creatine, blood-urea nitrogen and urea. These treatments significantly increased phosphorylation of survival kinases PI3K/Akt and ERK-1/2 and decreased the level of stress kinase JNK were noted. In addition, the activation level of signal transduction mediator p38 MAPK phosphorylation was higher particularly in both three-day DR groups. Next, animals were fed with carbohydrate-, protein- or fat-enriched diets in the presence of CP. Results indicated that not only fasting but also dietary content itself may play a determinant role in the severity of CPN. Our data suggest that DR is a promising approach to reduce CPN by regulating metabolism and cell signaling pathways.

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Objective: The aim of the study was to investigate the role of montelukast (ML), a cysteinyl leukotriene-1 receptor antagonist, on the water avoidance stress (WAS)induced degeneration of the rat urinary bladder mucosa. Methods: In WAS group, rats were exposed to WAS two hours daily for five days. In WAS+ML group, rats were administered ML (10 mg/kg; i.p.;) following every WAS exposure for 5 days. In control group, rats were injected vehicle solution only. The urinary bladder was evaluated for general morphology at light microscope. Mast cell activation and uroplakin distribution were assessed with immunohistochemistry. Glycosaminoglycan (GAG) distribution and urothelial permeability were observed using ruthenium red (RR) staining techniques in transmission electron microscope and luminal urothelial cells were observed with scanning electron microscope. Tissue malondialdehyde (MDA) and gluthatione (GSH) levels were also analysed. Results: Irregular GAG layer and uroplakin distribution, penetration of RR in the intercellular spaces and dilated tight junctions in urothelial layer, increase in inflammatory cell infiltration, in number of both granulated and activated mast cells, and were observed in the WAS group. The MDA level was increased, and GSH level was decreased significantly in urinary bladder in the WAS group in comparison with the control group. Quite regular GAG layer, uroplakin distribution and tight junctions in most regions, decrease in inflammatory cell infiltration and both of activated and granulated mast cells in the mucosa, were observed in WAS+ML group. Moreover, significant decrease in MDA and increase in GSH levels were observed in this group. Conclusion: Montelukast appears to exert a protective activity in WAS induced urinary bladder injury by inhibiting inflammatory and oxidative activity.