CAJ | 학술논문

目的：探讨脂肪来源间充质干细胞（ADMSC）在克罗恩病（CD）治疗中的作用及可能的作用机制。方法采用三硝基苯磺酸（TNBS）法建立CD小鼠动物模型。将75只6～8周龄SPF级雌性BALB／c小鼠，随机分成3组，包括对照组（乙醇溶液灌肠加PBS腹腔注射）、TNBS组（TNBS灌肠加PBS腹腔注射）和ADMSC组（TNBS灌肠加ADMSC腹腔注射），每组25只。通过免疫组织化学染色和实时定量 PCR等方法检测组织炎性细胞因子的水平，并记录各组小鼠生存曲线。结果 ADMSC组较TNBS组病变程度明显减轻，生存率明显增加（60％比30％，P＜0．05）。ADMSC组促炎因子坏死因子α（TNF-α）、白介素12（IL-12）及血管内皮生长因子（VEGF）的表达显著低于TNBS组，而抑炎因子IL-10的表达显著增加（均P＜0．05）。结论 ADMSC可能通过下调促炎因子TNF-α、IL-12和VEGF的表达和上调抑炎因子IL-10的表达，有效修复结肠炎性损伤，有望用于CD的临床治疗。
목적：탐토지방래원간충질간세포（ADMSC）재극라은병（CD）치료중적작용급가능적작용궤제。방법채용삼초기분광산（TNBS）법건립CD소서동물모형。장75지6～8주령SPF급자성BALB／c소서，수궤분성3조，포괄대조조（을순용액관장가PBS복강주사）、TNBS조（TNBS관장가PBS복강주사）화ADMSC조（TNBS관장가ADMSC복강주사），매조25지。통과면역조직화학염색화실시정량 PCR등방법검측조직염성세포인자적수평，병기록각조소서생존곡선。결과 ADMSC조교TNBS조병변정도명현감경，생존솔명현증가（60％비30％，P＜0．05）。ADMSC조촉염인자배사인자α（TNF-α）、백개소12（IL-12）급혈관내피생장인자（VEGF）적표체현저저우TNBS조，이억염인자IL-10적표체현저증가（균P＜0．05）。결론 ADMSC가능통과하조촉염인자TNF-α、IL-12화VEGF적표체화상조억염인자IL-10적표체，유효수복결장염성손상，유망용우CD적림상치료。
Objective To explore the efficacy of adipose-derived mesenchymal stem cells (ADMSCs) in a murine model of inflammatory bowel disease, and its potential mechanism. Methods Murine colitis mouse model of Crohn′s disease (CD) was created by trinitrobenzene sulfonic acid (TNBS)-induced colitis. Seventy-five 6-8 weeks female BALB/c mice were randomly divided into 3 groups: control group, TNBS group and ADMSC group. To verify the therapeutic effect of ADMSC, real-time PCR and immunohistochemical staining were performed to measure inflammatory cytokines levels in colon tissues. The 10-day survival statuses were recorded after the infusion of ADMSCs. Results Intraperitoneal injection of ADMSCs alleviated the clinical and histopathologic severity of intestinal inflammation, and increased survival(60% vs. 30%, P<0.05) in the TNBS-induced mouse model of CD. Compared with TNBS group, proinflammatory cytokines, including TNF-α, IL-12 and VEGF of ADMSC group were significantly reduced, with significant increase of IL-10 expression. Conclusion ADMSCs can effectively repair the injury of colonitis through down-regulation of proinflammatory cytokines TNF-α, IL-12 and VEGF expression, and up-regulation of anti-inflammatory cytokine IL-10 expression, which may be a potential new alternative of cell-based therapy for CD.