Protective effect of platelet-rich plasma on urethral injury model of male rats.

AIMS: Urethral stricture (US) formation is caused by fibrosis after excessive collagen formation following an injury or trauma to the urethra. In this study, we aimed to evaluate the effects of platelet-rich plasma (PRP) on a urethral injury (UI) model of male rats. METHODS: A UI model was used by applying a coagulation current to the urethras of male rats. There were four groups with six rats in each: control group, PRP applied to naive urethra, UI group, and UI with PRP application. PRP was applied to the urethra after a coagulation current-induced injury as soon as possible. On the 14th day, all rats were sacrificed and urethral tissues were investigated for collagen type I, collagen type III, platelet-derived growth factor-α, platelet-derived growth factor-ß, and transforming growth factor-ß using quantitative real-time polymerase chain reaction and Western blot analysis. The effect of urethral damage and healing was evaluated for collagen type I-to-collagen type III ratio. RESULTS: The collagen type I-to-collagen type III ratio was significantly higher in UI group (P < 0.05) than in the others, while UI with PRP application group had comparable results with the control group (P > 0.05). CONCLUSIONS: The results of this study show that PRP has a preventive effect on stricture formation in a UI model of rats, as shown by its effect on collagen synthesis. Further studies that eventually show the effects of PRP on human tissues are necessary and promising.

Halofuginone improves caustic-induced oxidative injury of esophagus in rats.

BACKGROUND: The aim of this study is to evaluate the anti-inflammatory and anti-fibrotic effects of halofuginone in caustic esophageal burn injury in rats. MATERIALS AND METHODS: Corrosive esophageal injury (CEI) was produced in male Wistar albino rats by instilling NaOH solution (1 ml, 37.5%) into the distal esophagus. Rats were decapitated on the 3rd day (early group) or 28th day (late group), and treated daily with either saline or halofuginone (100 µg/kg/day; i.p.), continued on alternate days after the third day. Histopathological evaluation and measurement of nitric oxide (NO), peroxynitrite (ONOO-) and oxygen-derived radicals by chemiluminescence (CL) were made in the distal 2 cm of the esophagus. Non-irrigated proximal esophageal samples were assessed for the levels of nuclear factor (NF)-κB, caspase-3, glutathione (GSH), malondialdehyde (MDA) and myeloperoxidase (MPO) activity. RESULTS: GSH, MDA, NF-κB and caspase-3 levels, and MPO activity in the proximal esophagus were not different among groups. Increased number of TUNEL (+) cells in the irrigated esophagus of the early and late caustic injury groups was reduced by halofuginone treatment. High microscopic damage scores in both early and late CEI groups were decreased with halofuginone treatment. NO, ONOO- and CL levels, which were elevated in the saline-treated early CEI group, were reduced by halofuginone treatment, but reduced NO and ONOO- levels in the late period of saline-treated group were increased by halofuginone. CONCLUSION: In addition to its anti-fibrotic effects, current findings demonstrate that halofuginone exerts antioxidant and anti-apoptotic actions and supports therapeutic potential for halofuginone in CEI-induced oxidative stress.