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

Journal of Biomedical Science

Durga Prasad Mishra⁶  Bhaskar Narayan²  Shivali Duggal⁶  Shio Kumar Singh⁴  Ratan Singh Ray¹  Hari Narayan Kushwaha⁴  Manjunatha Prabhu BH⁶  Shakir Ali³  Priyanka Gupta⁶  Namrata Rastogi⁶  Manish Kumar Pal⁵  Ashish Dwivedi¹  Amit Kumar Tripathi³ 

[1] Photobiology Division, Indian Institute of Toxicology Research, MG Marg, Lucknow 226001, India;Department of Meat, Fish & Poultry Technology, CSIR-Central Food Technological Research Institute, Mysore 570 020, India;Department of Biochemistry, Jamia Hamdard (Hamdard University, New Delhi, India;Pharmacokinetics and Metabolism Division, CSIR-Central Drug Research Institute, Lucknow 226031, India;Department of Obstetrics and Gynaecology, KGMU, Lucknow 226003, UP, India;Division of Endocrinology, CSIR-Central Drug Research Institute, Jankipuram Extension, Lucknow 226031, India

关键词: Neuroprotection;    C-jun;    miR-203;    UV-B;    Riboflavin;    Cerebral ischemia;   

Others  :  817638
DOI  :  10.1186/1423-0127-21-39

 received in 2013-11-17, accepted in 2014-04-15,  发布年份 2014

【 摘 要 】

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.

【 授权许可】

   
2014 Tripathi et al.; licensee BioMed Central Ltd.

【 图 表 】

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