研究人源性脂肪干细胞（h-ADSCs）对30%体表总面积（TBSA）Ⅲ度烫伤大鼠肺组织炎症反应的作用及机制。

采用随机数字表法将72只雄性Sprague-Dawley大鼠分为单纯烫伤组和h-ADSCs组，每组各36只。采用沸水水浴法制备30%TBSAⅢ度烫伤模型，烫伤后即刻，h-ADSCs组予尾静脉注射含600万h-ADSCs（总注射量约1 mL），单纯烫伤组予尾静脉注射等体积的等渗NaCl溶液。比较两组大鼠烫伤8 h、1周、2周后肺组织肿瘤坏死因子α（TNF-α）、白细胞介素6（IL-6）、α7烟碱型乙酰胆碱受体（α7nAChR）信使RNA（mRNA）及其蛋白、核因子κB（NF-κB）P65蛋白、苏木素-伊红（HE）染色评分及肺损伤评分，并在普通光镜下观察肺组织病理变化情况。

h-ADSCs组大鼠烫伤8 h、1周、2周后肺组织TNF-α（t=2.421、2.626、2.356，P=0.035、0.041、0.032）、IL-6（t=2.514、2.751、2.756，P=0.029、0.031、0.039）、HE染色评分（t=2.869、2.631、2.813，P=0.028、0.031、0.042）和肺损伤评分（t=2.172、3.017、2.698，P=0.033、0.032、0.029）和烫伤1周、2周后NF-κB P65蛋白（t=2.639、2.491，P=0.028、0.037）均明显低于单纯烫伤组同时间点；而烫伤1周、2周后α7nAChR mRNA（t=2.912、2.663，P=0.032、0.046）及其蛋白（t=2.814、2.638，P=0.033、0.032）表达水平均明显高于单纯烫伤组同时间点。伤后8 h，h-ADSC组大鼠肺泡隔增宽，间质血管充血，病变轻于单纯烫伤组。伤后1周，h-ADSCs组大鼠镜下可见肺间隔明显增厚，肺泡腔变窄，伴有炎症细胞浸润。伤后2周，h-ADSCs组大鼠镜下可见肺间隔明显增厚，肺泡腔变窄，伴有大量炎症细胞浸润。

h-ADSCs能减轻30%TBSA Ⅲ度烫伤休克大鼠肺组织炎症水平，其机制可能与h-ADSCs能增加α7nAChR的表达和抑制肺组织NF-κB P65的表达有关。

To investigate the effect and mechanism of human adipose-derived stem cells (h-ADSCs) on pulmonary inflammatory response in rats with 30% total body surface area (TBSA) third-degree scald.

A total of 72 male Sprague-Dawley rats were randomly assigned to a pure scald group and an h-ADSCs group (36 rats in each group). Using the boiling water bath method, rats in the two groups were subjected to 30% TBSA third-degree full-thickness thermal injury. Then rats in the h-ADSCs group received intravenous injection with 6 million h-ADSCs (the total injection volume is about 1 mL), and rats in the pure scald group received intravenous injection with an equal volume of saline. The tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), α7 nicotinic acetylcholine receptor (α7nAChR) messenger RNA (mRNA) and protein, nuclear factor-kappaB (NF-κB) P65 protein, hematoxylin-eosin (HE) staining score and lung injury score were compared between the two groups at 8 h, 1 week and 2 weeks after scald, and the pathological changes of lung tissue were observed under ordinary light microscope.

The TNF-α (t = 2.421, 2.626, 2.356; P = 0.035, 0.041, 0.032), IL-6 (t = 2.514, 2.751, 2.756; P = 0.029, 0.031, 0.039), HE staining score (t = 2.869, 2.631, 2.813; P = 0.028, 0.031, 0.042) and lung injury score (t = 2.172, 3.017, 2.698; P = 0.033, 0.032, 0.029) after 8 h, 1 week and 2 weeks of scald, and the NF-κB P65 protein (t = 2.639, 2.491; P = 0.028, 0.037) after 1 week and 2 weeks of scald in the h-ADSCs group were significantly lower than those in the pure scald group. After 1 week and 2 weeks of scald, the expressions of α7nAChR mRNA (t = 2.912, 2.663; P = 0.032, 0.046) and protein (t = 2.814, 2.638; P = 0.033, 0.032) in the h-ADSCs group were significantly higher than those in the pure scald group. At 8 h after injury, rats had wider alveolar septum, more stromal vascular congestion and fewer lesions in the h-ADSC group than in the pure scald group. One week after injury, rats in the h-ADSCs group showed significant thickened pulmonary septum and narrowed alveolar space with inflammatory cell infiltration. Two weeks after injury, rats in the h-ADSCs group showed significant thickened pulmonary septum and narrowed alveolar space with massive inflammatory cell infiltration.

The h-ADSCs can reduce the inflammation level of lung tissue in rats with 30% TBSA third-degree scald shock. These protective effects may be related to the increasing expressions of α7nAChR and decreasing expressions of NF-κB P65.