YKL-40，也称为几丁质酶-3-like-1 (CHI3L1)，是一种人软骨糖蛋白-39，其 N 末端由酪氨酸 (Y)、赖氨酸 (K) 和亮氨酸 (L) 组成，因此名称YKL-40。本研究探讨YKL-40是否能够促进Ⅱ型肺泡上皮细胞炎症因子的表达。将A549细胞与白介素（IL）-1β（20 ng/mL）、IL-6（20 ng/mL）一起体外培养。 /mL)、肿瘤坏死因子-α (TNF-α) (20 ng/mL) 和干扰素-γ (IFN-γ) (20 ng/mL)。通过RT-qPCR测定YKL-40转录的表达。将 A549 细胞与 5、10 和 20 ng/mL 的 IL-1β 一起培养，并通过 Western blot 测定 YKL-40 蛋白的表达。将重组 YKL-40 蛋白分别以 0、100、500 和 1 000 ng/mL 培养 A549 细胞，并通过 RT-qPCR 检测 IL-6 和 IL-8 的表达水平。设计三对靶向YKL-40的小干扰RNA（si-YKL-40-1/2/3）和阴性对照（NC），分别转染A549细胞，测定YKL-40的表达量通过 RT-qPCR 和蛋白质印迹。筛选出si-YKL-40-3用于后续实验。在A549细胞中，转染si-YKL-40-3和si-NC，然后加入IL-1β(20ng/mL)进行培养。 RT-qPCR法测定YKL-40、IL-6、IL-8的表达量，QAH-INF-1试剂盒测定上清液中多种因子的表达量。RT-qPCR结果显示IL-1β与对照组相比，IL-6、TNF-α、IFN-γ不能上调 YKL-40 蛋白转录水平，差异有统计学意义（ P<0.01）。蛋白质转录水平。 Western blot结果显示，IL-1β（20 ng/mL）能够显着促进YKL-40的表达，且与对照组相比，不同浓度IL-1β处理组的差异均具有统计学意义。 （P<0.01）。在 A549 细胞中添加人重组 YKL-40 蛋白后，结果显示，炎症因子 IL-6、IL-8 的表达量显着升高，与对照组相比，差异有统计学意义（ P<0.05）。 si-YKL-40-3 转染降低 YKL-40 表达后，IL-6（ P<0.05）、IL-8（ P<0.05）等炎症因子表达较对照组降低。 YKL-40可促进Ⅱ型肺泡上皮细胞模型A549细胞系IL-6、IL-8等急性炎症因子的表达和分泌，从而加重炎症反应。靶向抑制YKL-40表达可有效抑制炎症反应。四川大学学报（医学版）编委会版权所有©。

YKL-40, also known as chitinase-3-like-1 (CHI3L1), is a human cartilage glycoprotein-39, with its N-terminus consisting of tyrosine (Y), lysine (K), and leucine (L), hence the name YKL-40. In this study, we explored whether YKL-40 could promote the expression of inflammatory factors in type Ⅱ alveolar epithelial cells.A549 cells were cultured in vitro with interleukin (IL)-1β (20 ng/mL), IL-6 (20 ng/mL), tumor necrosis factor-alpha (TNF-α) (20 ng/mL), and interferon-gamma (IFN-γ) (20 ng/mL). The expression of YKL-40 transcription was determined by RT-qPCR. A549 cells were cultured with IL-1β at 5, 10, and 20 ng/mL and the expression of YKL-40 protein was determined by Western blot. A549 cells were cultured with recombinant YKL-40 protein at 0, 100, 500, and 1 000 ng/mL and the expression levels of IL-6 and IL-8 were measured by RT-qPCR. Three pairs of small interfering RNAs targeting YKL-40 (si- YKL-40-1/2/3) and the negative control (NC) were designed and used to transfect A549 cells, respectively, and the expression of YKL-40 was determined by RT-qPCR and Western blot. si- YKL-40-3 was screened out for subsequent experiments. In A549 cells, si- YKL-40-3 and si-NC were transfected and, then, IL-1β (20 ng/mL) was added in for culturing. The expression of YKL-40, IL-6, and IL-8 was determined by RT-qPCR and the expression of multiple factors in the supernatant was measured with the QAH-INF-1 kit.RT-qPCR results showed that IL-1β could up-regulate YKL-40 protein transcription level compared with that of the control group and the difference was statistically significant ( P<0.01), but IL-6, TNF-α, and IFN-γ could not up-regulate YKL-40 protein transcription level. Western blot results showed that IL-1β (20 ng/mL) could significantly promote the expression of YKL-40 and, compared with that of the control group, the differences showed by groups treated with different concentrations of IL-1β were all statistical significant ( P<0.01). After adding human recombinant YKL-40 protein to A549 cells, the results showed that the expression of inflammatory factors IL-6 and IL-8 was significantly increased and the difference was statistically significant compared with that of the control group ( P<0.05). After the expression of YKL-40 was decreased by si- YKL-40-3 transfection, the expression of IL-6 ( P<0.05), IL-8 ( P<0.05), and other inflammatory factors was inhibited compared with that of the control group.YKL-40 can promote the expression and secretion of IL-6, IL-8, and other acute inflammatory factors in A549 cell line, a type Ⅱ alveolar epithelial cell model, thus aggravating the inflammatory response. Targeted inhibition of YKL-40 expression may effectively inhibit inflammatory response.Copyright© by Editorial Board of Journal of Sichuan University (Medical Sciences).