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Introduction: Sialic acid plays pivotal roles in various critical physiological events at molecular and cellular levels and also pathological processes. Changes in sialic acid concentration are observed in many pathological processes; for example, there are some available data on the evaluated level of sialic acid and neurodegenerative prevalence. It can be proposed that sialic acid can play a significant role in the regulation of a diverse range of uncovered neurodegeneration factors and downstream targets. Matrix metalloproteinases 9 (MMP9) is one of these factors that changed in the exposure of different concentrations of sialic acid solution. Hence, in the current study, we aimed to examine the possible impact of sialic acid solution exposure in the glial cell line on the expression patterns of  miR-320a and let-7e as two upstream factors.
Materials and methods: Human glial cell line was prepared from the Pasteur Institute of Iran and was cultured in a DMEM medium with 10% FBS. The IC50 value of sialic acid was obtained by MTT assay, and the glial cell line was treated with sialic acid in 300µg/ ml, 500µg/ ml, 1000 µg/ ml for 24h to investigate the effect of the sialic acid ligand on the expression pattern of the miR-320a and let-7e. Total RNA was isolated from approximately 10 × 106 glial cells and was used from each sample for cDNA synthesis. For quantitative analysis of the miR-320a and the let-7e, we used real-time PCR, and for statistical analysis, the SPSS 21 software was applied.
Results: Analyzing of Real-time data revealed that expression of the miR-320a and let-7e expression was significantly increased (P<0.0001) in 300µg/ ml, 500µg/ ml, 1000 µg/ ml treated glial cells by sialic acid compared to the control group.
Conclusions: These findings have indicated a possible linkage of sialic acid on miR-320a and let-7e regulation in Glial cell line as pro-inflammatory factors in the inflammation pathway.
نوع مطالعه: Original | موضوع مقاله: Cellular and molecular Neuroscience
دریافت: 1398/7/8 | پذیرش: 1399/7/19

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