Interleukin (IL)-35, which has an anti-inflammatory role in acute respiratory distress syndrome (ARDS)/acute lung injury (ALI), is relatively promising as a drug target. Studies have shown that curcumin may play a therapeutic role in ALI and enhance the suppressive function of regulatory T cells (Tregs). To illustrate the effect of curcumin on the regulation of Treg cell differentiation and expression of IL-35, we built a cecal ligation and puncture (CLP)–induced acute lung injury mouse mode with curcumin pretreatment. The expression of IL-35 in serum, severity of lung injury, IL-17A in lung tissue, survival rate, Treg-related cytokines levels in serum, nuclear factor-kappa B (NF-κB)’s nuclear translocation in lung tissue, and splenic CD4+CD25+FOXP3+ Tregs were assessed. Furthermore, the proportion of Tregs, STAT5, and IL-35 expression during naïve CD4+ T cell differentiation in vitro was measured. Compared with the CLP group, the increased IL-35 expression in CLP with the curcumin pretreatment (CLP + Cur) group was consistent with the decreased severity of lung injury, IL-17A protein levels in lung tissue, and Treg-related cytokines levels. Pretreatment with curcumin, the survival rate climbed to 50%, while the mortality rate was 100% in the CLP group. In addition, splenic CD4+CD25+FOXP3+ Treg cells increased in the CLP + Cur group. In vitro, CD4+CD25+FOXP3+ Treg cells from naïve CD4+ T cells, STAT5 proportion, and IL-35 expression increased after curcumin treatment. These findings showed that curcumin might regulate IL-35 by activating the differentiation of Treg cells to control the inflammation in acute lung injury.

在急性呼吸窘迫综合征（ARDS）/急性肺损伤（ALI）中具有抗炎作用的白介素（IL）-35作为药物靶标相对有希望。研究表明姜黄素可能在ALI中起治疗作用，并增强调节性T细胞（Tregs）的抑制功能。为了说明姜黄素对Treg细胞分化和IL-35表达的调节作用，我们建立了盲肠结扎和穿刺（CLP）诱导的急性姜黄素预处理小鼠急性肺损伤模型。血清中IL-35的表达，肺损伤的严重程度，肺组织中的IL-17A，存活率，血清中Treg相关的细胞因子水平，肺组织中核因子-κB（NF-κB）的核易位，并评估脾脏CD4 + CD25 + FOXP3 + Treg。此外，Treg，STAT5，体外测量。与CLP组相比，姜黄素预处理（CLP + Cur）组在CLP中增加的IL-35表达与肺损伤严重程度降低，肺组织中IL-17A蛋白水平以及Treg相关细胞因子水平降低相符。用姜黄素预处理后，存活率攀升至50％，而CLP组的死亡率为100％。另外，CLP + Cur组脾脏CD4 + CD25 + FOXP3 + Treg细胞增加。在体外，姜黄素处理后，来自原始CD4 + T细胞的CD4 + CD25 + FOXP3 + Treg细胞，STAT5比例和IL-35表达增加。这些发现表明姜黄素可能通过激活Treg细胞的分化来控制IL-35，从而控制急性肺损伤中的炎症。