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Vitamin C Loaded Albumin Nanoparticles Treatment and Its Effect on Collagen I and III and mir-133 Genes Expression | ||
Journal of Cell and Molecular Research | ||
مقاله 11، دوره 13، شماره 1 - شماره پیاپی 25، آذر 2021، صفحه 92-97 اصل مقاله (641.7 K) | ||
نوع مقاله: Research Articles | ||
شناسه دیجیتال (DOI): 10.22067/jcmr.2021.71443.1011 | ||
نویسندگان | ||
Hamid Reza Shojania1؛ Madjid Momeni Moghaddam* 2؛ Seyed Ebrahim Hossini3 | ||
1Department of Genetics, Marvdasht Branch, Islamic Azad University, Marvdasht, Iran | ||
2Department of Biology, Faculty of Sciences, Hakim Sabzevari University, Sabzevar, Iran | ||
33Department of Biology, Faculty of Sciences, Zand Institute of Higher Education, Shiraz, Iran | ||
چکیده | ||
Wound healing is a complex biological process in which many molecules, including microRNA molecules, play an essential role in its regulation. It is well-established that reducing miR-155 expression can accelerate wound healing. This study investigated the effect of using nanoparticles loaded with vitamin C on miR-133, collagen I, and III expressions. In this study, first, nanoparticles of albumin protein were produced and then loaded with vitamin C. 3T3 mouse fibroblast cells were affected by these nanoparticles, and cell behavior was investigated to evaluate the toxicity and appropriate doses. In addition, the expression of collagen I and III genes was studied. The results showed that nanoparticles containing vitamin C in 20 µg/ml concentration had a positive effect on collagen I and III expressions compared to the control group. Moreover, we observed a decrease in the expression of miR-133 in comparison to the control group. Therefore, according to the results of this study, it can be argued that nanoparticles containing vitamin C can significantly decrease the expression of the miR-133 gene and lead to collagen I and III gene overexpression in fibroblasts cells, which is directly effective in wound healing. | ||
کلیدواژهها | ||
Wound Healing؛ Collagen I؛ Collagen III؛ MiR-133؛ Vitamin C | ||
مراجع | ||
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