Investigation of healing strategies in a rat corneal opacity model with polychromatic light and stem cells injection.

Corneal opacities are a major cause of vision loss worldwide. However, the current therapies are suboptimal to manage the corneal wound healing process. Therefore, there is an obvious need to develop new treatment strategies that are efficient in promoting wound healing in patients with severe corneal disorders. In this study, we investigated and compared the efficacy of adipose-derived mesenchymal stem cells (ADMSCs) and photobiomodulation (PBM) with polychromatic light in the NIR (600-1200 nm) alone and in combination, on corneal opacity, inflammatory response, and tissue architecture in a rat corneal opacity model created by mechanical injury. All animals were divided into four groups randomly following the injury: injury only (no treatment), ADMSCs treatment, PBM treatment and combined (ADMSCs+PBM) treatment (n = 12 eyes per group). At the 10th and 30th day following injury, corneal opacity formation, neovascularization, and corneal thickness were assessed. On the 30th day the harvested corneas were analyzed by transmission electron microscopy (TEM), histological evaluation, immunohistochemical (IHC) staining and real-time polymerase chain reaction (RT-PCR). On day 30, the corneal opacity score, neovascularization grade, and corneal thickness in all treatment groups were significantly lower in comparison with the untreated injured corneas. The TEM imaging and H&E staining together clearly revealed a significant enhancement in corneal regeneration with improved corneal microenvironment and reduced vascularization in the combined administration of PBM and ADMSCs compared to treatment of PBM and ADMSCs alone. In addition, the IHC staining, and RT-PCR analysis supported our hypothesis that combining ADMSCs therapy with PBM alleviated the inflammatory response, and significantly decreased scar formation compared to either ADMSCs or PBM alone during the corneal wound healing.

The effects of melatonin on possible damage that will occur on adipocytokines and liver tissue by coadministration of fructose and bisphenol a (BPA).

BPA, one of the environmental endocrine disruptors, and fructose, reason of liver steatosis which is frequently encountered in the daily diet, contribute to the formation of metabolic syndrome (MetS). This study examines the possible effects of concurrent fructose and BPA administration on MetS and determines the effects of melatonin on this process. In the seven identified groups, a total of forty-two adult male Sprague Dawley rats were treated by following fructose, BPA, and melatonin amounts, separately and together: group 1 (control), group 2 (10% aqueous fructose), group 3 (25 mg/kg BPA), group 4 (10% fructose + 25 mg/kg BPA), group 5 (10% fructose + 20 mg/kg melatonin), group 6 (25 mg/kg BPA + 20 mg/kg melatonin), and group 7 (10% fructose + 25 mg/kg BPA + 20 mg/kg melatonin). At the end of 60 days, histochemical, immunohistochemical, and biochemical procedures were performed on liver tissue. As a result, it was seen that BPA and fructose + BPA induced morphological alteration and inflammation and increased intracellular lipid quantity and amount of collagen and reticular fibers. The percentage of apoptotic liver cells stained by annexin V-FITC/PI was lower in group 7 compared to the group 4 (p < 0,001) and also in group 6 compared to the group 3 (p = 0.014). Both BPA and fructose application caused an increase in lipid peroxidation level due to the increase of oxidative stress. Application of melatonin induced antioxidant enzyme activity and reduced lipid peroxidation level. Our results indicate that fructose and BPA administration triggered the formation of MetS, whereas melatonin healed these variations, although not entirely.

Possible effects of melatonin against rat uterus exposure to bisphenol A during neonatal period.

The aim of this study was to investigate the possible effects of melatonin on rat uterine tissue against exposure with bisphenol A (BPA) in the neonatal period. Twenty-four female rats were divided into four groups, (n=6) per group. Group I was used as a control (sesame oil + ethanol), group II was injected daily with (100 mg/kg) BPA by subcutaneously (sc) daily postnatal days (PND 0-10), group III was injected daily with (10 mg/kg) melatonin by sc for 10 days (PND 20-30), and group IV was injected daily with (100 mg/kg) BPA (PND 0-10) and (10 mg/kg) melatonin (PND 20-30). All rats were sacrificed in the same day of metestrus cycle, approximately PND 70. Histological analyses, immunostaining of B cell lymphoma 2 (Bcl-2), and cytochrome c and TUNEL assays were performed. According to our results, neonatal exposure to BPA accelerates onset of puberty, causes degenerative and morphometric changes on rat uterus, and increases apoptotic reaction rates. The immunoreactivity of Bcl-2 was decreased after BPA administration. In addition, immunoreactivity of Bcl-2 showed an increase after melatonin treatment. However, cytochrome c immunoreactivity was decreased after melatonin administration. Our results suggest that melatonin may have positive effects against BPA-induced degenerative changes on rat uterus.