Oral mucositis (OM) is characterized by the presence of severe ulcers in the oral region that affects patients treated with chemotherapy. It occurs in almost all patients who receive radiotherapy of the head and neck, as well as patients who undergo hematopoietic cell transplantation. The pathophysiology of OM is complex, and there is no effective therapy. The aim of this study was to evaluate the effect of dexamethasone-loaded poly(d,l-Lactic-co-glycolic) nanoparticles (PLGA-DEX NPs) on an OM model induced in hamsters. The NPs were synthesized using the emulsification-solvent evaporation method and were characterized by the size, zeta potential, encapsulation efficiency, atomic force microscopy, physicochemical stability, and the in vitro release. The OM was induced by the administration of 5-FU on the first and second days and mechanical trauma on the 4th day of the experiment. PLGA-DEX NPs were administered to treat OM. The animals were euthanized on the 10th day. Macroscopic and histopathological analyses were performed, measurement of malonaldehyde (MDA) and ELISA was used to determine the levels of IL-1β and TNF-α. Immunoexpressions of NF-κB, COX-2, and TGF-β were determined by immunohistochemistry, and qRT-PCR was used to quantify the gene expression of the GILZ, MKP1, and NF-κB p65. The PLGA-DEX NPs (0.1 mg/kg) significantly reduced macroscopic and histopathological scores, decreased MDA, TNF-α and IL-1β levels, immunostaining for NF-κB, COX-2, TGF-β, and suppressed NF-κB p65 mRNA expression, but increased GILZ and MKP1 expression.

Background: Oral mucositis (OM) is a severe inflammation of the oral mucosal cells associated with chemotherapy and/or radiotherapy-induced toxicity, resulting in epithelial ulcers and higher risk of death from sepsis. The aim of the present study was to evaluate the nanoparticle (AuNp) effect on OM induced in hamsters. Materials and methods: 5-fluorouracil (5FU) was used on the first and second day of the experimental model in Golden sirian hamsters, and on the fourth day, mechanical trauma was applied to induce OM. The animals were divided into groups, i.e., polyvinylpyrrolidone (PVP), mechanical trauma (MT), 5FU, and groups treated with gold nanoparticles (AuNps) (62.5, 125, and 250 μg/kg). On the 10th day, animals were euthanized for macroscopic, histopathological, immunohistochemical, western blot, quantitative polymerase chain reaction (qRT-PCR), and AuNp quantification. Results: AuNp (250 μg/kg) reduced TNF-α, IL-1β, COX-2, NF-κB, TGF-β, and SMAD 2/3; increased glutathione levels; decreased the expression of Kelch ECH-associated protein 1 (KEAP1); and induced heme oxygenase 1 (HMOX-1) and NAD (P) H quinone oxidoreductase 1 (NQO1) genes. Conclusions: AuNp (250 μg/kg) prevented 5-FU-induced OM in hamsters and improved the parameters of inflammation and oxidative stress.

The clinical advantages of light-emitting diode (LED) therapy in skin healing and its underlying mechanism remain subjects of ongoing debate. This study aims to explore the impact of LED therapy on normal skin keratinocytes (HaCaT) and in the repair of full-thickness dorsal wounds in Wistar rats. HaCaT cell viability (SRB assay) and migration (scratch assay) were assessed under LED therapy, comparing stress conditions (2.5% FBS) with sham irradiation and optimal conditions (10% FBS). In vivo, 50 rats with induced wounds were divided into Sham and LED (daily treatment) groups. Euthanasia occurred at 3, 5, 10, 14, and 21 days for clinical, morphological, oxidative stress (MDA, SOD, and GSH), and cytokine analyses (IL-1β, IL-10, TNF-α). LED therapy significantly enhanced keratinocytes viability compared to sham irradiation, with minimal impact on cell migration. Clinical benefits were prominent on day 10, influencing inflammation progression and resolution on days 3 and 10. Re-epithelization remained unaffected. Reduced MDA and increased GSH levels were observed throughout, while SOD levels varied temporally. Notably, on day 10, LED significantly decreased IL-1β, IL-10, and TNF-α. Although translational, clinical trial confirmation of observed benefits is warranted. LED therapy expedites cutaneous healing in the experimental model, primarily modulating inflammation and enhancing antioxidant activity.

Purpose: This study aimed to evaluate the effect of oral administration of a hydroethanolic extract of Commiphora leptophloeos leaves (CLF) on the progression of 5-fluorouracil (5-FU)-induced intestinal mucositis. Methods: Female Swiss mice were orally administered CLF at doses of 10, 100, or 300 mg/kg, or saline (negative control, NC), starting 30 minutes before intraperitoneal injection of 5-FU. A positive control (PC) group received 5-FU without CLF treatment. Treatment continued until euthanasia, three days after 5-FU injection. Body weight was monitored throughout the experiment. On day 4, small intestine tissue samples were collected for histopathological analysis. Duodenal tissue was also assessed for Muc-2 immunostaining. Results: In the CLF 10, 100 and 300 mg/kg groups, the duodenum histopathological score was 1 (1–1.5) p < 0.001, 1 (1–1.5) p < 0.01; 1 (1–1.25) p < 0.01, while the PC group score was 2 (2–2.75). Immunostaining analysis for Muc-2 revealed a score of 3 (3–3) in the CLF 10 group, compared to score 1.2 (0.8–1.6) in the PC group (p < 0.001), indicating that CLF 10 increased Muc-2 expression. Conclusion: The oral administration of a hydroethanolic extract of CLF protected the duodenal segment of Swiss mice from 5-FU-induced intestinal mucositis, likely by increasing mucin production.

The obesogenic nutrient composition and processing characteristics of ultra-processed foods may contribute to metabolic dysfunction. The present study evaluated a standardized cafeteria diet, alone or combined with low-dose streptozotocin (STZ), in male Wistar rats. Animals (n = 32) were allocated to Healthy Control, STZ (35 mg/kg), Cafeteria Diet (CAF), and CAF + STZ groups. The diet contained standard chow, condensed milk, refined sugar, hydrogenated fat, soybean oil, and chocolate-filled biscuits, homogenized and thermally processed at 180°C. After 102 days, anthropometric, metabolic, inflammatory, gene expression, microbiota, and histopathological parameters were assessed. CAF induced a marked obesogenic phenotype, with increased body weight (+172.3%) and abdominal circumference (+38.7%; P < 0.01). CAF showed hyperglycemia (median glucose, 403 mg/dl) and higher HOMA-IR than Healthy Control (P < 0.01); CAF + STZ also showed increased HOMA-IR (P < 0.05). CAF increased IL-1β and IL-6 (P < 0.05), triglycerides, adipocyte hypertrophy (P < 0.01), and adipose leptin expression (P < 0.05), while reducing muscle Slc2a4/GLUT4 expression (P < 0.01). Liver, kidney, and pancreatic histopathological scores did not differ significantly. Gut microbiota showed marked compositional imbalance and low taxonomic evenness, with Firmicutes (99.83%), Ligilactobacillus (99.36%), and Lactobacillaceae (99.52%) predominating, while Enterobacteriaceae represented 0.14%. Despite no reduction in Shannon or Simpson indices, extreme Ligilactobacillus dominance indicated a restricted and uneven community. Overall, the cafeteria diet reproduced obesity-associated metabolic dysfunction, characterized by hyperglycemia, insulin resistance, inflammation, adipocyte hypertrophy, altered glucose and leptin expression, and substantial microbiota restructuring.