Abstract—The aim of this work was to study the effects of thymosin-1 alpha (Tα1) on the anti-inflammatory response of RAW 264.7 macrophages cultured in the presence of lipopolysaccharide (LPS) from the walls of gram-negative bacteria. As well, we evaluated production of pro-inflammatory cytokines and the activity of the NF-κB and SAPK/JNK signaling pathways. In addition, the level of expression of a number of genes that regulate cell apoptosis, as well as the activity of receptors involved in the pro-inflammatory response, was determined. First, the addition of Tα1 normalized the level of cytokine production to varying degrees, with a particularly noticeable effect on IL-1β and IL-6. Second, the addition of Tα1 normalized the activity of the NF-κB and SAPK/JNK signaling cascades and the expression of the Tlr4 gene. Third, Tα1 significantly reduced p53 and the activity of the P53 gene, which is a marker of cell apoptosis. Fourth, it was shown that the increase in Ar-1 gene expression under the influence of LPS was significantly reduced using Tα1. Thus, it was found that the presence of Tα1 in the RAW 264.7 cell culture medium significantly reduced the level of the pro-inflammatory response of cells.

摘要：本工作的目的是研究胸腺肽 1 α (Tα1) 对在革兰氏阴性菌壁脂多糖 (LPS) 存在下培养的 RAW 264.7 巨噬细胞抗炎反应的影响。此外，我们还评估了促炎细胞因子的产生以及 NF-κB 和 SAPK/JNK 信号通路的活性。此外，还测定了许多调节细胞凋亡的基因的表达水平，以及参与促炎症反应的受体的活性。首先，Tα1 的添加在不同程度上使细胞因子的产生水平正常化，对 IL-1β 和 IL-6 的影响尤其明显。其次，Tα1 的添加使 NF-κB 和 SAPK/JNK 信号级联的活性以及Tlr4基因的表达正常化。第三，Tα1显着降低p53和P53基因的活性，P53基因是细胞凋亡的标志。第四，表明使用Tα1显着降低了LPS影响下Ar-1基因表达的增加。因此，发现RAW 264.7细胞培养基中Tα1的存在显着降低了细胞的促炎反应水平。