[ 摘 要 ] 目的：探讨粪肠球菌脂磷壁酸（lipoteichoic acid，LTA）对胰腺导管腺癌（pancreatic ductal adenocarcinoma，PDA） BxPC3 细胞增殖、侵袭和迁移的影响及其可能的机制。方法：用 0、5、10、50 μg/ml 的 LTA 分别处理 BxPC-3 细胞，以 0 μg/ml 组作为空白对照组，其余各组作为实验组，采用 CCK-8 法检测 LTA 对细胞 BxPC-3 增殖的影响；用 50 μg/ml LTA 处理 BxPC-3 细胞 48 h，采用划痕实验和 Transwell 小室实验分别检测其对 BxPC-3 细胞侵袭和迁移的影响，WB 法检测对 BxPC3 细 胞中 TLR2、P38、p-P38、NF-κB 和 p-NF-κB 蛋白表达的影响。结果：LTA 抑制 BxPC3 细胞的增殖，且抑制作用随时间和浓度的 增加而增强，与 0 μg/ml 组相比，在 LTA 50 μg/ml 干预 48 h 后，BxPC-3 细胞增殖抑制效果最为显著（P<0.01），故后续实验组细胞均采用 50 μg/ml LTA 处理 48 h。与 0 μg/ml 组相比，50 μg/ml 组发生侵袭的 BxPC-3 细胞数和迁移率均显著降低（均 P<0.01），细胞中 TLR2、p-P38、p-NF-κB 蛋白水平均显著升高（均 P<0.01）。结论：粪肠球菌 LTA 可抑制 PDA 细胞 BxPC-3 的增殖、侵袭和迁移， 其机制可能与 LTA 激活 TLR2 进而促进 P38 及 NF-κB 磷酸化有关。

[Abstract] Objective: To investigate the effect of Enterococcus faecalis lipoteichoic acid (LTA) on the proliferation, invasion and migration of pancreatic ductal adenocarcinoma (PDA) cell line BxPC-3 and its possible mechanism. Methods: BxPC-3 cells were treated with 0, 5, 10 and 50 μg/ml LTA; the 0 μg/ml group was set as the blank control group, while the other groups were used as the experimental groups. CCK-8 method was used to detect the effect of LTA on the proliferation of BxPC-3 cells. BxPC-3 cells were treated with 50 μg/ml LTA for 48 h, and the invasion and migration abilities of BxPC-3 cells were detected by the Scratch test and Transwell chamber test, respectively. WB assay was used to detect the effect of LTA on protein expression of TLR2, P38, p-P38, NF-κB and p-NF-κB in BxPC-3 cells. Results: LTA inhibited the proliferation of BxPC-3 cells, and the inhibitory effect increased with time and concentration. Compared with the 0 μg/ml group, LTA at 50 μg/ml exhibited the most significant inhibitory effect on proliferation of BxPC-3 cells after 48 h (P<0.01); thus, the subsequent experimental groups were treated with 50 μg/ml LTA for 48 h. Compared with the 0 μg/ml group, the number of invaded cells and the migration rate of BxPC-3 cells in the 50 μg/ml group were significantly reduced (all P<0.01), and the protein expression levels of TLR2, p-P38 and p-NF-κB were significantly increased (all P<0.01). Conclusion: Enterococcus faecalis LTA can inhibit the proliferation, invasion and migration of pancreatic cancer BxPC-3 cells. The mechanism may be related to the activation of TLR2 by LTA to promote phosphorylation of P38 and NF-κB.