Acute lung injury (ALI) is a pathologic condition responsible for incurable human chronic respiratory diseases. Recent studies have shown the involvement of the glycoprotein, IL17A secreted by IL-17 producing cells in chronic inflammation. The current investigation was carried out to study the IL-17A mediated activation of SMAD and non- SMAD signaling in alveolar epithelial cells and to assess the putative modulatory role of curcumin. C57BL/6 mice were exposed to IL-17A and curcumin was administered as an intervention to modulate the IL-17A-induced alveolar damage. Techniques like Immunofluorescence and real-time PCR were used. We found elevated expression of IL-17A and IL-17A—associated signaling pathways to be activated in mice lung tissues. Curcumin intervention in vivo promoted the resolution of IL-17A-induced ALI and attenuated pulmonary damage. Increase phosphorylation of non- SMAD proteins like P-EGFR, P-STAT-1, STAT-3, P-JAK-1/2, P-JNK, and also SMAD proteins like P- SMAD 2/3 and TGF-β1 was encountered upon IL-17A exposure, while curcumin intervention reversed the protein expression levels. Curcumin was found to block mRNA expressions of non- SMAD genes EGFR, JNK-1, JAK1, JAK2, STAT-1, STAT-3, MAPK14, also of TGF-β1 and SMAD genes like SMAD 2, SMAD 3. However, mRNA expressions of SMAD 6 and SMAD 7 were increased upon curcumin intervention. Our study indicates that IL-17A participates in the development of ALI in both SMAD dependent and independent manner and the IL-17A signaling components were effectively controlled by curcumin, suggesting probable anti-inflammatory use of curcumin during ALI.

急性肺损伤（ALI）是导致无法治愈的人类慢性呼吸道疾病的病理状况。最近的研究表明，由IL-17产生细胞分泌的糖蛋白IL17A与慢性炎症有关。目前的研究是为了研究IL-17A介导的肺泡上皮细胞中SMAD和非SMAD信号的激活，并评估姜黄素的假定调节作用。将C57BL / 6小鼠暴露于IL-17A，并给予姜黄素作为干预措施，以调节IL-17A诱导的肺泡损伤。使用了免疫荧光和实时PCR等技术。我们发现IL-17A和IL-17A相关信号通路在小鼠肺组织中的表达升高。姜黄素的体内干预促进了IL-17A诱导的ALI的消退并减轻了肺损伤。非SMAD蛋白（如P-EGFR，P-STAT-1，STAT-3，P-JAK-1 / 2，P-JNK）以及SMAD蛋白（如P-SMAD 2/3和TGF-β1）的磷酸化增加在暴露于IL-17A时会遇到这种情况，而姜黄素干预会逆转蛋白质表达水平。发现姜黄素可阻断非SMAD基因EGFR，JNK-1，JAK1，JAK2，STAT-1，STAT-3，MAPK14的mRNA表达，也可阻断TGF-β1和SMAD基因（如SMAD 2，SMAD 3）的mRNA表达。姜黄素干预后SMAD 6和SMAD 7的表达增加。我们的研究表明，IL-17A以SMAD依赖和独立方式参与ALI的发展，姜黄素可有效控制IL-17A信号传导成分，