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首页> 外文期刊>Bangladesh Journal of Medical Science >UVB Dose Optimization for Phototherapy in Vitamin D Deficiency : Profile Analysis of Vitamin D, TNF-α, Vascular Endothelial Growth Factor (VEGF) and Platelet Derived Growth Factor (PDGF) in Wistar Rats
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UVB Dose Optimization for Phototherapy in Vitamin D Deficiency : Profile Analysis of Vitamin D, TNF-α, Vascular Endothelial Growth Factor (VEGF) and Platelet Derived Growth Factor (PDGF) in Wistar Rats

机译:维生素D缺乏光疗法的UVB剂量优化:Wistar大鼠中维生素D,TNF-α,血管内皮生长因子(VEGF)和血小板衍生生长因子(PDGF)的概况分析

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Background : UVB radiation responsible for the most important biological effects including Vitamin D3 synthesis and inflammation. UVB radiation are absorbed by 7-dehydrocholesterol in the plasma membrane of epidermal cells resulting in production of cis-previtamin D3. In the other hand, an exposure to UVB leads to cutaneous tissue inflammation modulates by TNF-α which also increases platelet activating factor. VEGF and PDGF induced by TNF-α during wound healing, characterized with angiogenesis and reephitalization. Furthermore, vitamin D plays a role in inflammation inhibition and upregulates growth factors. However, the study of the mechanism has not yet been thoroughly investigated. Methods : This study uses post test only group design, subjected wistar rats divided into four groups. Control group, non irradiated with UVB, and the other three groups, treated with graded UVB dose started with 1 MED (50 mJ/cm2), 2 MED (100mJ/cm2) and 3 MED (150 mJ/cm2) and investigated at 6, 12, 24 and 48 hours post UVB irradiation. Result : The serum level of vitamin D, VEGF and PDGF were increasing due to UVB dose addition. The highest level was reached at 6 hours post radiation using 3 MED, which gradually decrease up to 48 hours (p =0,000). The rise of vitamin D after UVB radiation, inhibit TNF-α induction in every dose accordant UVB dose addition and the lowest level is using 3 MED at 12 hours post radiation (p =0,000). TNF-α reach its highest level at 24 hours post radiation using 1 MED, it is related with the acute phase of inflammation. Conclusion : This study reveal that higher UVB irradiance increases vitamin D and inhibit TNF-α which also promotes VEGF and PDGF.
机译:背景:UVB辐射负责最重要的生物效应,包括维生素D3合成和炎症。通过在表皮细胞的质膜膜中吸收uvB辐射,其表皮细胞的质膜导致CIS-PREMITOMIN D3的产生。另一方面,暴露于UVB导致皮肤组织炎症通过TNF-α调节,这也增加了血小板活化因子。 TNF-α在伤口愈合过程中诱导的VEGF和PDGF,其特征在于血管生成和重新计算。此外,维生素D在炎症抑制和上调生长因子中起作用。然而,对机制的研究尚未得到彻底调查。方法:本研究仅使用后检测仅群体设计,受到的Wistar大鼠分为四组。用渐变UVB剂量处理的对照组,非辐射,与其他三组,用1MED(50mJ / cm2),2MED(100MJ / CM2)和3MED(150mJ / cm2)进行,并在6中进行研究UVB辐照后12,24和48小时。结果:由于UVB剂量添加,维生素D,VEGF和PDGF的血清水平越来越大。使用3个MED后6小时达到最高水平,逐渐减少至48小时(P = 0,000)。维生素D在UVB辐射之后的升高,抑制每种剂量均衡的UVB剂量添加的TNF-α诱导,最低水平在辐射后12小时使用3 mEC(P = 0,000)。 TNF-α在使用1 med后24小时后达到其最高水平,它与炎症的急性阶段有关。结论:本研究表明,较高的UVB辐照度增加了维生素D并抑制TNF-α,其还促进VEGF和PDGF。

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