Attenuated neuroprotective effect of riboflavin under UV-B irradiation via miR-203/c-Jun signaling pathway in vivo and in vitro

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• 作者：Amit Kumar Tripathi (1) (4)
  Ashish Dwivedi (2)
  Manish Kumar Pal (3)
  Namrata Rastogi (1)
  Priyanka Gupta (1)
  Shakir Ali (4)
  Manjunatha Prabhu BH (1)
  Hari Narayan Kushwaha (5)
  Ratan Singh Ray (2)
  Shio Kumar Singh (5)
  Shivali Duggal (1)
  Bhaskar Narayan (6)
  Durga Prasad Mishra (1)
  
  1. Division of Endocrinology ; CSIR-Central Drug Research Institute ; Jankipuram Extension ; Lucknow ; 226031 ; India
  4. Department of Biochemistry ; Jamia Hamdard (Hamdard University ; New Delhi ; India
  2. Photobiology Division ; Indian Institute of Toxicology Research ; MG Marg ; Lucknow ; 226001 ; India
  3. Department of Obstetrics and Gynaecology ; KGMU ; Lucknow ; 226003 ; UP ; India
  5. Pharmacokinetics and Metabolism Division ; CSIR-Central Drug Research Institute ; Lucknow ; 226031 ; India
  6. Department of Meat ; Fish & Poultry Technology ; CSIR-Central Food Technological Research Institute ; Mysore ; 570 020 ; India
  
• 关键词：Cerebral ischemia ; Riboflavin ; UV ; B ; miR ; 203 ; C ; jun ; Neuroprotection
• 刊名：Journal of Biomedical Science
• 出版年：2014
• 出版时间：December 2014
• 年：2014
• 卷：21
• 期：1
• 全文大小：704 KB
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• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Biomedicine
  
• 出版者：Springer Netherlands
• ISSN：1423-0127

文摘

Background Riboflavin (RF) or vitamin B2 is known to have neuroprotective effects. In the present study, we report the attenuation of the neuroprotective effects of RF under UV-B irradiation. Preconditioning of UV-B irradiated riboflavin (UV-B-RF) showed attenuated neuroprotective effects compared to that of RF in SH-SY5Y neuroblostoma cell line and primary cortical neurons in vitro and a rat model of cerebral ischemia in vivo. Results Results indicated that RF pretreatment significantly inhibited cell death and reduced LDH secretion compared to that of the UV-B-RF pretreatment in primary cortical neuron cultures subjected to oxygen glucose deprivation in vitro and cortical brain tissue subjected to ischemic injury in vivo. Further mechanistic studies using cortical neuron cultures revealed that RF treatment induced increased miR-203 expression which in turn inhibited c-Jun expression and increased neuronal cell survival. Functional assays clearly demonstrated that the UV-B-RF preconditioning failed to sustain the increased expression of miR-203 and the decreased levels of c-Jun, mediating the neuroprotective effects of RF. UV-B irradiation attenuated the neuroprotective effects of RF through modulation of the miR-203/c-Jun signaling pathway. Conclusion Thus, the ability of UV-B to serve as a modulator of this neuroprotective signaling pathway warrants further studies into its role as a regulator of other cytoprotective/neuroprotective signaling pathways.