Yang Jia, Liu Yang, Wang Minghui, Chen Shengqin, Miao Qingya, Liu Zhicong, Zhang Bin, Deng Guodong
Guangdong Provincial Key Laboratory of Marine Biotechnology, Department of Biology, College of Science, Shantou University, Shantou 515063, China.
Polymers (Basel). 2024 Jun 28;16(13):1845. doi: 10.3390/polym16131845.
Umbilical cord mesenchymal stem cells (UC-MSCs) possess the capabilities of differentiation and immune modulation, which endow them with therapeutic potential in the treatment of type 2 diabetes mellitus (T2DM). In this study, to investigate the repair mechanism of UC-MSCs in hydrogel on pancreatic β-cells in diabetes, mouse insulinoma 6 (MIN-6) cells damaged by streptozotocin (STZ) in vitro were used in co-culture with UC-MSCs in hydrogel (UC-MSCs + hydrogel). It was found that UC-MSCs + hydrogel had a significant repair effect on injured MIN-6 cells, which was better than the use of UC-MSCs alone (without hydrogel). After repair, the expression of superoxide dismutase (SOD) and catalase (CAT) as well as the total antioxidant capacity (T-AOC) of the repaired MIN-6 cells were increased, effectively reducing the oxidative stress caused by STZ. In addition, UC-MSCs + hydrogel were able to curb the inflammatory response by promoting the expression of anti-inflammatory factor IL-10 and reducing inflammatory factor IL-1β. In addition, the expression of both nuclear antigen Ki67 for cell proliferation and insulin-related genes such as and was increased in the repaired MIN-6 cells by UC-MSCs + hydrogel, suggesting that the repair effect promotes the proliferation of the injured MIN-6 cells. Compared with the use of UC-MSCs alone, UC-MSCs + hydrogel exhibit superior antioxidant stress resistance against injured MIN-6 cells, better proliferation effects and a longer survival time of UC-MSCs because the porous structure and hydrophilic properties of the hydrogel could affect the growth of cells and slow down their metabolic activities, resulting in a better repair effect on the injured MIN-6 cells.
脐带间充质干细胞（UC-MSCs）具有分化和免疫调节能力，这使其在治疗2型糖尿病（T2DM）方面具有治疗潜力。在本研究中，为了探究水凝胶中的UC-MSCs对糖尿病胰腺β细胞的修复机制，将体外被链脲佐菌素（STZ）损伤的小鼠胰岛素瘤6（MIN-6）细胞与水凝胶中的UC-MSCs（UC-MSCs + 水凝胶）进行共培养。结果发现，UC-MSCs + 水凝胶对受损的MIN-6细胞具有显著的修复作用，优于单独使用UC-MSCs（无水凝胶）。修复后，修复的MIN-6细胞中超氧化物歧化酶（SOD）和过氧化氢酶（CAT）的表达以及总抗氧化能力（T-AOC）均增加，有效降低了STZ引起的氧化应激。此外，UC-MSCs + 水凝胶能够通过促进抗炎因子IL-10的表达和减少炎症因子IL-1β来抑制炎症反应。另外，UC-MSCs + 水凝胶使修复的MIN-6细胞中细胞增殖核抗原Ki67以及胰岛素相关基因如 和 的表达均增加，表明这种修复作用促进了受损MIN-6细胞的增殖。与单独使用UC-MSCs相比，UC-MSCs + 水凝胶对受损的MIN-6细胞表现出更强的抗氧化应激能力、更好的增殖效果以及UC-MSCs更长的存活时间，因为水凝胶的多孔结构和亲水特性会影响细胞生长并减缓其代谢活动，从而对受损的MIN-6细胞产生更好的修复效果。
