背景:受体部位的血液灌注对于脂肪移植后的脂肪组织修复很重要。其递送源自骨髓中单核细胞的宿主衍生的巨噬细胞以引发炎症反应和再生反应。根据CXCL12,基质细胞衍生因子的能力,招募单核细胞/巨噬细胞,我们研究了其在缺血和正常条件下对脂肪组织修复和再生的影响。
方法:在小鼠(n=35)中,用夹子将每个腹股沟脂肪垫压碎30秒。将左腹股沟血管分开并切断(缺血组),而右侧腹股沟血管保持开放(对照组)。在手术后1、3、7、14和30天处死7只动物,和巨噬细胞(Mac2和CD206)和脂肪细胞(perilipin)进行评估。炎症因子(白细胞介素(IL)-1β,通过定量PCR测量IL-6,肿瘤坏死因子-α)和CXCL12。
结果:第3天,对照组的巨噬细胞数量高于缺血组(10.33±2.40vs.1.33±0.33,p=0.021)。在第7天,对照组的M2巨噬细胞百分比高于缺血组(p<0.05)。早期对照组炎症因子和CXCL12水平高于缺血组(p=0.038)。
结论:建立的血液灌注导致脂肪组织修复和再生过程中CXCL12的上调,这可能会增加单核细胞对受损脂肪组织的募集。这些发现增加了对移植后脂肪移植物存活所涉及的细胞事件的理解。
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BACKGROUND: Blood perfusion in the recipient site is important for adipose tissue repair after fat grafting. It delivers host-derived macrophages derived from monocytes in bone marrow to initiate inflammatory reactions and regenerative responses. According to the ability of CXCL12, a stromal cell-derived factor, to recruit monocytes/macrophages, we studied its effect on adipose tissue repair and regeneration under ischemic and normal conditions.
METHODS: Each inguinal fat pad was crushed for 30 seconds with a clamp in mice (n = 35). The left inguinal vessels were divided and cut off (ischemic group), while the right inguinal vessels were kept patent (control group). Seven animals were sacrificed at 1, 3, 7, 14, and 30 days after surgery, and macrophages (Mac2 and CD206) and adipocytes (perilipin) were assessed. Levels of inflammatory factors (interleukin (IL)-1β, IL-6, and tumor necrosis factor-α) and CXCL12 were measured by quantitative PCR.
RESULTS: The number of macrophages was higher in the control group than in the ischemic group at day 3 (10.33 ± 2.40 vs. 1.33 ± 0.33, p = 0.021). The percentage of M2 macrophages was higher in the control group than in the ischemic group at day 7 (p<0.05). The levels of inflammatory factors and CXCL12 were higher in the control group than in the ischemic group at the early stage (p = 0.038).
CONCLUSIONS: Established blood perfusion leads to up-regulation of CXCL12 during adipose tissue repair and regeneration, which may increase recruitment of monocytes to damaged adipose tissue. These findings increase understanding of the cellular events involved in fat graft survival after grafting.
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