Background:Recent studies have shown that BMSCs have a putative ability to promote neurogenesis and produce behavioral and functional improvement. Our previous study demonstrated that co-treatment of G-CSF and BMSCs have beneficial effects on Parkinson's models. The main purpose of this research was to investigate the effects of these two factors on oxidative stress factors in the brain of Parkinson's rat. Methods: Adult male Wistar rats (weighing 200-250 g) were used and randomly divided into five groups of seven each. To create the Parkinson's model, 6-OHDA was injected into the left SNpc. The BMSCs (2 × 10 6 ) and G-CSF (75 µg/kg) were used for treatment after creating the PD model. After four weeks, the brains of rats were removed and processed for immunohistochemical studies, such as TH-positive neurons as well as analysis of oxidative stress factors. Results:The results showed that the injected BMSCs could cross the BBB. The injected cells are also able to settle in different areas of the brain. Analyses of the brain oxidative stress factors showed that G-CSF and BMSCs reduced the expression of MDA and induced the activity of SOD, GSH-Px, and FRAP. Conclusion: Co-administration of G-CSF and BMSCs reduced the expression of pro-inflammatory cytokines and induced the activity of antioxidant enzymes; however, neurogenesis increased in the brain.
Some growth factors, such as Epidermal Growth Factor (EGF), Growth Hormone (GH) and Platelet Derived Growth Factor (PDGF) have beneficial effects on keratinocyte proliferation and wound healing. Although the mechanism of these factors is unclear. In response to injury, growth factors are secreted by kinds of cutaneous cells. The goal of this project is to investigate the factors that could cause proliferate of the keratinocyte cells in vitro. The keratinocytes were removed from rat pups (10 days). Cultured in media with different concentration of GH, PDGF and EGF separately. The proliferation of cells was evaluated by the method of MTT and 3H-thymidine incorporation. Proliferation of keratinocytes was significantly higher in experimental groups than in control group. EGF maximally stimulated at 10 and 25 ng mL(-1). PDGF-BB maximally stimulated at 50 ng mL(-1), respectively. And maximal stimulation of GH was 2.5 IU L(-1). GH, PDGF-BB and EGF stimulate keratinocyte cells proliferation in different concentration. These growth factors could play in healing of the skin.
Background: Many studies have shown that polyvinyl chloride (PVC) has toxic effects on the body and brain. Vitamin E is a nutritional supplement that acts as an antioxidant, scavenging toxic free radicals. Objectives: The aim of this study was to examine the protective effects of vitamin E against PVC-induced damages in rat hippocampus. Methods: In this study, 24 male Wistar rats were randomly divided to four groups (n = 6), including control, vitamin E (150 mg/kg.bw/day), PVC (1000 mg/kg.bw/day), PVC + vitamin E. The administration routes were oral and the experiment period was 40 days. At the end of the examination, rats were euthanized and the brain was removed and the left hippocampus was transferred to 10% formalin for H-E staining, TUNNEL, and crystal violet. Data were analyzed by SPSS 24 software and Tukey's test. Results: The present results showed that oral administration of PVC was associated with an increase in apoptosis in the hippocampus. vitamin E led to suppression of apoptosis in the hippocampus of rats. Conclusions: Exposure to PVC can cause hippocampus damage, while vitamin E, as an antioxidant, may reduce the destructive effects of PVC in rat hippocampus.
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