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目的:探讨炎性牙周膜干细胞（periodontal ligament stem cell，PDLSC）对巨噬细胞分泌白介素-1β（interleukin-1β，IL-1β）的影响及其机制。方法:使用脂多糖（lipopolysaccharide，LPS）刺激PDLSC模拟炎性环境。收集健康PDLSC培养基和模拟炎性环境条件PDLSC培养基，分别作用于人单核细胞系THP-1细胞，以此分为健康PDLSC条件培养基（conditioned medium of health PDLSC，CM-H）组和炎性PDLSC条件培养基（conditioned medium of LPS-PDLSC，CM-LPS）组。条件培养24 h后，弃条件培养基，正常培养THP-1细胞24 h。酶联免疫吸附测定（enzyme linked immunosorbent assay，ELISA）法检测THP-1细胞上清液中IL-1β的表达量，实时荧光定量PCR检测THP-1细胞内质网应激（endoplasmic reticulum stress，ERS）相关基因葡萄糖调节蛋白78（glucose regulated protein 78，GRP78）、活化转录因子6（activating transcription factor-6，ATF6）、需肌醇酶1（inositol requiring enzyme 1，IRE1）、蛋白激酶R样内质网激酶（protein kinase R-like endoplasmic reticulum kinase，PERK）、CCAAT增强子结合蛋白同源蛋白（CCAAT enhancer binding protein homologous protein，CHOP）、活化转录因子4 （activating transcription factor-4，ATF4）、剪切型X-盒结合蛋白1（X box binding protein 1 spliced，XBP1s）的表达，蛋白质印迹法检测GRP78、CHOP蛋白表达。使用ERS抑制剂4-苯基丁酸（4-phenylbutyrate，4-PBA）预处理THP-1细胞进行干预实验，以不同浓度进行分组，包括0（对照组）、1、10和20 mmol/L组，检测ERS相关基因mRNA表达和IL-1β分泌的变化。结果:ELISA结果显示，CM-LPS组THP-1细胞IL-1β表达量［（31.35±2.11） ng/L］显著高于CM-H组［（8.19±1.51） ng/L］（n t=12.60，n P<0.01）。实时荧光定量PCR结果显示，与CM-H组相比，CM-LPS组GRP78、ATF6、IRE1、PERK、CHOP、ATF4、XBP1s表达（分别为1.782±0.070、1.387±0.204、1.404±0.119、1.777±0.187、1.325±0.156、1.295±0.066、1.137±0.149）均显著升高（n P<0.05）。4-PBA干预实验中，1、10、20 mmol/L组中GRP78、IRE1、ATF6、PERK、CHOP的表达均显著低于对照组（n P<0.05）。与对照组［（31.23±1.98） ng/L］相比，10和20 mmol/L组THP-1细胞IL-1β分泌水平［分别为（21.20±0.37）、（23.85±1.80） ng/L］均显著下降（n P<0.05）。n 结论:炎性PDLSC可以通过上调巨噬细胞的ERS促进巨噬细胞分泌IL-1β。“,”Objective:To investigate the effect and mechanism of periodontal ligament stem cell (PDLSC) from inflammatory environment on the secretion of interleukin-1β (IL-1β) by macrophages.Methods:PDLSCs were pretreated with lipopolysaccharide (LPS) in order to simulate the inflammatory environment. Human monocyte cell line (THP-1) cells were treated with conditioned media collected from healthy and inflammatory PDLSCs respectively and divided into conditioned medium of health PDLSC (CM-H) group and conditioned medium of LPS-PDLSC (CM-LPS) group. After 24 h of co-culture, the condition media were abandoned and THP-1 cells were then cultured for another 24 h. The expression of IL-1β in THP-1 cells supernatant was detected by enzyme-linked immunosorbent assay (ELISA). Quantitative real time-PCR (qRT-PCR) was used to detect the expression of glucose regulated protein 78 (GRP78), activating transcription factor-6 (ATF6), inositol requiring enzyme 1 (IRE1), protein kinase R-like endoplasmic reticulum kinase (PERK), CCAAT enhancer binding protein homologous protein (CHOP), activating transcription factor-4 (ATF4) and X box binding protein 1 spliced (XBP1s), which were all related with endoplasmic reticulum stress (ERS), in THP-1 cells. The expressions of proteins GRP78 and CHOP were detected by Western blotting. Furthermore, THP-1 cells, which pretreated with ER inhibitor 4-phenylbutyrate (4-PBA) for intervention experiments were grouped by various concentrations of 4-PBA including groups 0 (control group), 1, 10 and 20 mmol/L and treated with condition medium of inflammatory PDLSC. ELISA was used to detect IL-1β expression and qRT-PCR to detect expression of ERS related genes.Results:ELISA results showed that the expression of IL-1β in THP-1 cells of group CM-LPS [(31.35±2.11) ng/L] was significantly higher than group CM-H [(8.19±1.51) ng/L] (n t=12.60, n P<0.01). qRT-PCR results showed that the relative expressions of GRP78, ATF6, IRE1, PERK, CHOP, ATF4 and XBP1s genes in THP-1 cells of group CM-LPS (1.782±0.070, 1.387±0.204, 1.404±0.119, 1.777±0.187, 1.325±0.156, 1.295±0.066 and 1.137±0.149, respectively) were significantly higher than those in group CM-H (n P<0.05). In the 4-PBA intervention experiment, compared with group 0 mmol/L, the expressions of GRP78, IRE-1, ATF-6, PERK and CHOP were significantly lower in group 1, 10 and 20 mmol/L (n P<0.05). Moreover, compared with control group [(31.23±1.98) ng/L], the expression of IL-1β in THP-1 cells were significantly lower in group 10 mmol/L [(21.20±0.37) ng/L] and group 20 mmol/L [(23.85±1.80) ng/L] (n P<0.05) with ERS inhibited.n Conclusions:PDLSC from inflammatory environment could promote IL-1β secretion of macrophages through upregulating macrophages ERS.