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Abstract Vitiligo, an acquired pigmentary disorder of the skin, is characterized by a chronic and progressive loss of melanocyte from the epidermis and follicular reservoir. Growth factor of surrounding cells impacted on melanocytes survival. In this study, lower level of IGF-1 in the lesion was found than that in the donor area of vitiligo patients. IGF-1 improved activation of Nrf2, and inhibited ROS generation and endoplasmic reticulum dilation in HaCaT. C57BL/6 mice were treated with 5% H 2 O 2 , and combined with 50 μg/kg of IGF-1 pre-treatment or not once every day for 50 consecutive days. After 50 days, IGF-1 obviously ameliorated depigmentation of mice skin and reduced hair follicle length, skin thickness and Tyrosinase induced by H 2 O 2. Moreover, IGF-1 significantly suppressed CD8+ T cells infiltration in mice skin, inhibited the production of IL-2 and IFN-γ, and decreased the expression of CXCL10 and CXCR3. Thus, the results indicated that IGF-1 could resist oxidative damage to HaCaT, suppress CD8+ T cells infiltration and pro-inflammatory cytokines secretion, and suppresses the thinning of epidermal layer in vivo. It suggests that IGF-1 inhibits oxidative damage to HaCaT and immunosuppressive effects on CD8+ T cells proliferation and activation to resist depigmentation induced by H 2 O 2. This disclosed its multiple roles in the vitiligo, and shed a light on developing the application potential for IGF-1 in vitiligo. [ABSTRACT FROM AUTHOR]

Abstract: Staphylococcal enterotoxin C injection is established as a clinical therapy for delayed healing or disunion of bone fractures. In the present study, the effects of staphylococcal enterotoxin C injection in combination with ascorbic acid (SEC-AA) on the differentiation of bone marrow-derived mesenchymal stem cells (MSCs) and their influences on the mineralization of osteoblasts were investigated. SEC-AA treatment induced increased levels of alkaline phosphatase activity in MSCs and increased numbers of alizarin red-stained calcified nodules, indicating enhanced differentiation of MSCs into osteoblasts. The findings demonstrated that SEC-AA promoted the differentiation of MSCs into osteoblasts and accelerated the cytopoiesis of osteoblasts. Our data provide a cytological model for bone fracture therapy aimed at shortening the time required for healing and improving the clinical outcome, and also provide a theoretical basis for inducible differentiation of MSCs, mineralization of osteoblasts and reconstruction of bone tissues. [Copyright &y& Elsevier]

The 21-amino acid-length endothelin-1 (ET-1)(1–21) and its novel derivative, 31 amino acid-length ET-1(1–31), have proinflammatory properties and induce significant eosinophil migration mediated by an increase in the local levels of eotaxin and IL-5. We have analyzed by reverse transcription polymerase chain reaction and enzyme immunoassay the effects of ETs on the expression of IL-13 mRNA and protein in eosinophils with or without cell priming with IL-5. The expression of the ETA receptor (ETAR) and its membrane localization were detected in the eosinophils, whereas the ETB receptor was undetectable. ET peptides synergistically increased the expression of IL-13 in eosinophils after priming with IL-5, and the increase was blocked by the ETAR antagonist BQ123, though these peptides did not directly influence the expression. These results may explain the presence of eosinophilia in the airways’ epithelium of patients suffering from asthma, along with an increase in immunoreactive ETs. [Copyright &y& Elsevier]

Abstract: Vascular endothelial growth factor (VEGF) was investigated in the present study to see whether it could provide a therapeutic opportunity for the treatment of Alzheimer’s disease (AD). PDGF-hAPPV717I transgenic mice were treated with VEGF or PBS by intraperitoneal injection for three consecutive days. The results showed that VEGF ameliorated the memory impairment of mice, accompanied by CD34+ cells increasing in peripheral blood, vWF+ vessels increasing in hippocampus, and CD34+/VEGFR2+, vWF+/VEGFR2+ and BrdU+/vWF+ cells expressing in hippocampus. Furthermore, the level of choline acetyltransferase (ChAT) was considerably enhanced and Aβ deposition was decreased in the brains of mice upon VEGF treatment. These observations suggest that VEGF should be pursued as a novel therapeutic agent for treatment of AD. [Copyright &y& Elsevier]