Influence of autologous adipose stem cell matrix gel on wound healing and scar hyperplasia of full-thickness skin defects in rabbit ears
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摘要:
目的 探讨自体脂肪干细胞基质胶对兔耳全层皮肤缺损创面愈合及瘢痕增生的影响，并分析其相关机制。 方法 采用实验研究方法。切取42只2~3个月龄雄性新西兰大白兔背部完整脂肪垫，制备脂肪干细胞基质胶，并于每只兔双耳腹侧制备全层皮肤缺损创面，将左耳创面纳入脂肪干细胞基质胶组（以下简称基质胶组）、右耳创面纳入磷酸盐缓冲液（PBS）组，分别注入自体脂肪干细胞基质胶和PBS。计算伤后7、14、21 d创面愈合率，并于创面愈合后1、2、3、4个月行创面形成瘢痕组织（以下简称瘢痕组织）温哥华瘢痕量表（VSS）评分；行苏木精-伊红染色观测伤后7、14、21 d创面组织病理学改变和创面愈合后1、2、3、4个月瘢痕组织真皮厚度；行Masson染色观察伤后7、14、21 d创面组织和创面愈合后1、2、3、4个月瘢痕组织中胶原排布，并计算胶原容积分数（CVF）；采用免疫组织化学法观测伤后7、14、21 d创面组织中微血管计数（MVC）与创面愈合后1、2、3、4个月瘢痕组织中转化生长因子-β1（TGF-β1）和α平滑肌肌动蛋白（α-SMA）的表达，并行基质胶组瘢痕组织中α-SMA与TGF-β1表达相关性分析；采用酶联免疫吸附测定法检测伤后7、14、21 d创面组织中血管内皮生长因子（VEGF）和表皮生长因子（EGF）的表达。各组各时间点样本数均为6。对数据行重复测量方差分析、析因设计方差分析、配对样本t检验、LSD检验与Pearson相关性分析。 结果 伤后7 d，基质胶组创面愈合率为（10.3±1.7）%，与PBS组的（8.5±2.1）%接近（P>0.05）；伤后14、21 d，基质胶组创面愈合率分别为（75.5±7.0）%、（98.7±0.8）%，均明显高于PBS组的（52.7±6.7）%、（90.5±1.7）%（t值分别为5.79、10.37，P<0.05）。创面愈合后1、2、3、4个月，基质胶组瘢痕组织VSS评分均明显低于PBS组（t值分别为-5.00、-2.86、-3.31、-4.45，P<0.05）。与组内前一时间点比较，除基质胶组创面愈合后4个月（P>0.05）外，2组创面愈合后各时间点瘢痕组织VSS评分均明显升高（P<0.05）。伤后7 d，2组创面肉芽组织再生与上皮化程度接近；伤后14、21 d，基质胶组创面组织中成纤维细胞、毛细血管、上皮细胞层数明显多于PBS组。创面愈合后1、2、3、4个月，基质胶组瘢痕组织真皮厚度均明显薄于PBS组（t值分别为-4.08、-5.52、-6.18、-6.30，P<0.05）。与组内前一时间点比较，2组创面愈合后各时间点瘢痕组织真皮厚度均明显增厚（P<0.05）。与PBS组比较，基质胶组伤后14、21 d创面组织中胶原排布更规则且CVF均明显升高（t值分别为3.98、3.19，P<0.05），创面愈合后1、2、3、4个月瘢痕组织中胶原排布也更规则但CVF均明显降低（t值分别为-7.38、-4.20、-4.10、-4.65，P<0.05）。与组内前一时间点比较，除基质胶组创面愈合后1个月（P>0.05）外，2组创面伤后各时间点创面组织与创面愈合后各时间点瘢痕组织中CVF均明显升高（P<0.05）。伤后14、21 d，基质胶组创面组织中MVC均明显高于PBS组（t值分别为4.33、10.10，P<0.05）。与组内前一时间点比较，除PBS组伤后21 d（P>0.05）外，2组创面伤后各时间点MVC均明显升高（P<0.05）。创面愈合后1、2、3、4个月，基质胶组瘢痕组织中TGF-β1和α-SMA的表达均明显低于PBS组（t值分别为-2.83、-5.46、-5.61、-8.63，-10.11、-5.79、-8.08、-11.96，P<0.05）。与组内前一时间点比较，除基质胶组创面愈合后4个月α-SMA表达（P>0.05）外，2组创面愈合后各时间点瘢痕组织中TGF-β1与α-SMA表达均明显升高（P<0.05）。基质胶组瘢痕组织中α-SMA与TGF-β1表达之间呈显著正相关（r=0.92，P<0.05）。伤后14、21 d，基质胶组创面组织中VEGF（t值分别为6.14、6.75，P<0.05）和EGF（t值分别为8.17、5.85，P<0.05）的表达均明显高于PBS组。与组内前一时间点比较，2组创面伤后各时间点VEGF表达均明显增高（P<0.05），EGF表达均明显下降（P<0.05）。 结论 脂肪干细胞基质胶可能通过促进创面组织中胶原沉积和VEGF、EGF的表达从而显著促进兔耳全层皮肤缺损创面愈合，还可能通过抑制瘢痕组织中胶原沉积和TGF-β1、α-SMA的表达进一步抑制创面愈合后瘢痕增生。 Abstract:Objective To investigate the influence of autologous adipose stem cell matrix gel on wound healing and scar hyperplasia of full-thickness skin defects in rabbit ears, and to analyze the related mechanism. Methods Experimental research methods were adopted. The complete fat pads on the back of 42 male New Zealand white rabbits aged 2 to 3 months were cut to prepare adipose stem cell matrix gel, and a full-thickness skin defect wound was established on the ventral side of each ear of each rabbit. The left ear wounds were included in adipose stem cell matrix gel group (hereinafter referred to as matrix gel group), and the right ear wounds were included in phosphate buffer solution (PBS) group, which were injected with autologous adipose stem cell matrix gel and PBS, respectively. The wound healing rate was calculated on post injury day (PID) 7, 14, and 21, and the Vancouver scar scale (VSS) scoring of scar tissue formed on the wound (hereinafter referred to as scar tissue) was performed in post wound healing month (PWHM) 1, 2, 3, and 4. Hematoxylin-eosin staining was performed to observe and measure the histopathological changes of wound on PID 7, 14, and 21 and the dermal thickness of scar tissue in PWHM 1, 2, 3, and 4. Masson staining was performed to observe the collagen distribution in wound tissue on PID 7, 14, and 21 and scar tissue in PWHM 1, 2, 3, and 4, and the collagen volume fraction (CVF) was calculated. The microvessel count (MVC) in wound tissue on PID 7, 14, and 21 and the expressions of transforming growth factor β1 (TGF-β1) and α smooth muscle actin (α-SMA) in scar tissue in PWHM 1, 2, 3, and 4 were detected by immunohistochemical method, and the correlation between the expression of α-SMA and that of TGF-β1 in scar tissue in matrix gel group was analyzed. The expressions of vascular endothelial growth factor (VEGF) and epidermal growth factor (EGF) in wound tissue were detected by enzyme-linked immunosorbent assay on PID 7, 14, and 21. The number of samples at each time point in each group was 6. Data were statistically analyzed with analysis of variance for repeated measurement, analysis of variance for factorial design, paired sample t test, least significant difference test, and Pearson correlation analysis. Results On PID 7, the wound healing rate in matrix gel group was (10.3±1.7)%, which was close to (8.5±2.1)% in PBS group (P>0.05). On PID 14 and 21, the wound healing rates in matrix gel group were (75.5±7.0)% and (98.7±0.8)%, respectively, which were significantly higher than (52.7±6.7)% and (90.5±1.7)% in PBS group (with t values of 5.79 and 10.37, respectively, P<0.05). In PWHM 1, 2, 3, and 4, the VSS score of scar tissue in matrix gel group was significantly lower than that in PBS group (with t values of -5.00, -2.86, -3.31, and -4.45, respectively, P<0.05). Compared with the previous time point within the group, the VSS score of scar tissue at each time point after wound healing in the two groups was significantly increased (P<0.05), except for PWHM 4 in matrix gel group (P>0.05). On PID 7, the granulation tissue regeneration and epithelialization degree of the wounds between the two groups were similar. On PID 14 and 21, the numbers of fibroblasts, capillaries, and epithelial cell layers in wound tissue of matrix gel group were significantly more than those in PBS group. In PWHM 1, 2, 3, and 4, the dermal thickness of scar tissue in matrix gel group was significantly thinner than that in PBS group (with t values of -4.08, -5.52, -6.18, and -6.30, respectively, P<0.05). Compared with the previous time point within the group, the dermal thickness of scar tissue in the two groups thickened significantly at each time point after wound healing (P<0.05). Compared with those in PBS group, the collagen distribution in wound tissue in matrix gel group was more regular and the CVF was significantly increased on PID 14 and 21 (with t values of 3.98 and 3.19, respectively, P<0.05), and the collagen distribution in scar tissue was also more regular in PWHM 1, 2, 3, and 4, but the CVF was significantly decreased (with t values of -7.38, -4.20, -4.10, and -4.65, respectively, P<0.05). Compared with the previous time point within the group, the CVFs in wound tissue at each time point after injury and scar tissue at each time point after wound healing in the two groups were significantly increased (P<0.05), except for PWHM 1 in matrix gel group (P>0.05). On PID 14 and 21, the MVC in wound tissue in matrix gel group was significantly higher than that in PBS group (with t values of 4.33 and 10.10, respectively, P<0.05). Compared with the previous time point within the group, the MVC of wound at each time point after injury in the two groups was increased significantly (P<0.05), except for PID 21 in PBS group (P>0.05). In PWHM 1, 2, 3, and 4, the expressions of TGF-β1 and α-SMA in scar tissue in matrix gel group were significantly lower than those in PBS group (with t values of -2.83, -5.46, -5.61, -8.63, -10.11, -5.79, -8.08, and -11.96, respectively, P<0.05). Compared with the previous time point within the group, the expressions of TGF-β1 and α-SMA in scar tissue in the two groups were increased significantly at each time point after wound healing (P<0.05), except for the α-SMA expression in matrix gel group in PWHM 4 (P>0.05). There was a significantly positive correlation between the expression of α-SMA and that of TGF-β1 in scar tissue in matrix gel group (r=0.92, P<0.05). On PID 14 and 21, the expressions of VEGF (with t values of 6.14 and 6.75, respectively, P<0.05) and EGF (with t values of 8.17 and 5.85, respectively, P<0.05) in wound tissue in matrix gel group were significantly higher than those in PBS group. Compared with the previous time point within the group, the expression of VEGF of wound at each time point after injury in the two groups was increased significantly (P<0.05), and the expression of EGF was decreased significantly (P<0.05). Conclusions Adipose stem cell matrix gel may significantly promote the wound healing of full-thickness skin defects in rabbit ears by promoting collagen deposition and expressions of VEGF and EGF in wound tissue, and may further inhibit the scar hyperplasia after wound healing by inhibiting collagen deposition and expressions of TGF-β1 and α-SMA in scar tissue. -
参考文献
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1 2组兔耳全层皮肤缺损创面伤后各时间点愈合情况。1A、1B、1C和1D、1E、1F.分别为磷酸盐缓冲液组和脂肪干细胞基质胶组伤后7、14、21 d创面，图1D与图1A创面大小接近，图1E较图1B创面明显缩小，图1F较图1C创面明显缩小且创面未结痂
2 2组兔耳全层皮肤缺损创面愈合后各时间点创面形成瘢痕组织增生情况。2A、2B、2C、2D和2E、2F、2G、2H.分别为磷酸盐缓冲液组与脂肪干细胞基质胶组创面愈合后1、2、3、4个月瘢痕组织，图2E、2F、2G、2H分别较图2A、2B、2C、2D瘢痕情况好，表现为颜色更浅、厚度更薄、血管分布更少
3 2组兔耳全层皮肤缺损创面伤后各时间点创面组织中CD34阳性微血管（棕色）情况 二氨基联苯胺×200。3A、3B、3C和3D、3E、3F.分别为磷酸盐缓冲液组和脂肪干细胞基质胶组伤后7、14、21 d创面组织，图3A和3D创面基底有少量新生微血管，图3B、3C、3E、3F创面基底有大量新生微血管，且图3E、3F微血管数量分别多于图3B、3C，图3F微血管数量多于图3E，图3B、3C微血管数量接近
4 2组兔耳全层皮肤缺损创面愈合后4个月创面形成瘢痕组织中转化生长因子β1（TGF-β1）与α平滑肌肌动蛋白（α-SMA）表达（均为棕色）情况 二氨基联苯胺×200。4A、4B.分别为磷酸盐缓冲液（PBS）组、脂肪干细胞基质胶组TGF-β1表达，均较多，图4B中TGF-β1表达少于图4A；4C、4D.分别为PBS组、脂肪干细胞基质胶组α-SMA表达，均较多，图4D中α-SMA表达少于图4C
表1 2组兔耳全层皮肤缺损创面伤后各时间点愈合率比较(%，
组别 样本数 7 d 14 d 21 d 磷酸盐缓冲液组 6 8.5±2.1 52.7±6.7 90.5±1.7 脂肪干细胞基质胶组 6 10.3±1.7 75.5±7.0 98.7±0.8 t值 1.57 5.79 10.37 P值 0.147 <0.001 <0.001 注：处理因素主效应，F=55.49,P<0.001；时间因素主效应，F=1 361.95,P<0.001；二者交互作用，F=21.41,P<0.001 
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表2 2组兔耳全层皮肤缺损创面愈合后各时间点创面形成瘢痕组织温哥华瘢痕量表评分比较(分，
组别 样本数 1个月 2个月 3个月 4个月 磷酸盐缓冲液组 6 6.0±0 8.2±0.8 10.3±1.0 12.2±1.5 脂肪干细胞基质胶组 6 5.2±0.4 7.2±0.4 8.8±0.4 9.3±0.5 t值 -5.00 -2.86 -3.31 -4.45 P值 0.004 0.017 0.008 0.004 P1值 — 0.001 0.001 0.004 P2值 — <0.001 <0.001 0.062 注：处理因素主效应，F=32.75,P<0.001；时间因素主效应，F=130.78,P<0.001；二者交互作用，F=5.24,P=0.005；t值、P值为组间比较所得，P1值、P2值分别为磷酸盐缓冲液组、脂肪干细胞基质胶组组内各时间点与前一时间点比较所得；“—”表示无此项
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表3 2组兔耳全层皮肤缺损创面愈合后各时间点创面形成瘢痕组织真皮厚度比较(mm，
组别 样本数 1个月 2个月 3个月 4个月 磷酸盐缓冲液组 6 0.98±0.05 1.45±0.07 1.88±0.09 2.20±0.09 脂肪干细胞基质胶组 6 0.85±0.06 1.26±0.05 1.61±0.05 1.94±0.04 t值 -4.08 -5.52 -6.18 -6.30 P值 0.002 <0.001 <0.001 <0.001 P1值 — <0.001 <0.001 <0.001 P2值 — <0.001 <0.001 <0.001 注：处理因素主效应，F=124.17,P<0.001；时间因素主效应，F=685.85,P<0.001；二者交互作用，F=2.85,P=0.049；t值、P值为组间比较所得，P1值、P2值分别为磷酸盐缓冲液组、脂肪干细胞基质胶组组内各时间点与前一时间点比较所得；“—”表示无此项
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表4 2组兔耳全层皮肤缺损创面伤后各时间点创面组织与愈合后各时间点创面形成瘢痕组织中胶原容积分数比较(%，
组别 样本数 伤后7 d 伤后14 d 伤后21 d 愈合后1个月 愈合后2个月 愈合后3个月 愈合后4个月 磷酸盐缓冲液组 6 51.9±0.6 55.1±1.2 59.4±1.1 67.5±1.1 70.7±1.5 73.5±1.0 76.8±1.9 脂肪干细胞基质胶组 6 52.2±1.1 58.1±1.4 61.7±1.3 62.2±1.4 66.5±1.9 68.8±2.6 71.3±2.2 t值 0.54 3.98 3.19 -7.38 -4.20 -4.10 -4.65 P值 0.605 0.003 0.010 <0.001 0.002 0.006 0.001 P1值 — <0.001 <0.001 <0.001 <0.001 0.001 <0.001 P2值 — <0.001 <0.001 0.599 <0.001 0.027 0.020 注：处理因素主效应，F=36.07,P<0.001；时间因素主效应，F=325.73,P<0.001；二者交互作用，F=17.60,P<0.001；t值、P值为组间比较所得，P1值、P2值分别为磷酸盐缓冲液组、脂肪干细胞基质胶组组内各时间点与前一时间点比较所得；“—”表示无此项
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表5 2组兔耳全层皮肤缺损创面伤后各时间点200倍视野下微血管计数比较（个，
组别 样本数 7 d 14 d 21 d 磷酸盐缓冲液组 6 6.8±1.5 15.7±2.9 17.5±1.8 脂肪干细胞基质胶组 6 7.3±1.1 25.0±4.4 32.6±3.2 t值 0.53 4.33 10.10 P值 0.610 0.001 <0.001 P1值 — <0.001 0.167 P2值 — <0.001 <0.001 注：处理因素主效应，F=82.79,P<0.001；时间因素主效应，F=140.71,P<0.001；二者交互作用，F=22.17,P<0.001；t值、P值为组间比较所得，P1值、P2值分别为磷酸盐缓冲液组、脂肪干细胞基质胶组组内各时间点与前一时间点比较所得；“—”表示无此项
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表6 2组兔耳全层皮肤缺损创面愈合后各时间点创面形成瘢痕组织中TGF-β1与α-SMA表达比较（
组别 样本数 TGF-β1 α-SMA 1个月 2个月 3个月 4个月 1个月 2个月 3个月 4个月 磷酸盐缓冲液组 6 0.050±0.006 0.065±0.003 0.089±0.008 0.103±0.006 0.078±0.004 0.112±0.009 0.157±0.008 0.170±0.008 脂肪干细胞基质胶组 6 0.041±0.005 0.052±0.005 0.068±0.005 0.075±0.005 0.059±0.003 0.086±0.007 0.121±0.008 0.127±0.008 t值 -2.83 -5.46 -5.61 -8.63 -10.11 -5.79 -8.08 -11.96 P值 0.018 <0.001 <0.001 0.001 <0.001 <0.001 <0.001 <0.001 P1值 — <0.001 <0.001 0.001 — <0.001 <0.001 0.007 P2值 — 0.001 <0.001 0.027 — <0.001 <0.001 0.080 注：转化生长因子-β1（TGF-β1）、α平滑肌肌动蛋白（α-SMA）处理因素主效应，F值分别为124.98、272.26,P值均<0.001；时间因素主效应，F值分别为151.80、386.57,P值均<0.001；二者交互作用，F值分别为7.10、8.05,P值分别为0.001、<0.001；t值、P值为组间比较所得，P1值、P2值分别为磷酸盐缓冲液组、脂肪干细胞基质胶组组内各时间点与前一时间点比较所得；“—”表示无此项
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表7 2组兔耳全层皮肤缺损创面伤后各时间点组织中VEGF和EGF表达比较（μg/L，
组别 样本数 VEGF EGF 7 d 14 d 21 d 7 d 14 d 21 d 磷酸盐缓冲液组 6 296±22 395±18 443±21 260±9 183±10 118±11 脂肪干细胞基质胶组 6 320±23 465±21 556±35 269±11 226±8 156±12 t值 1.89 6.14 6.75 1.39 8.17 5.85 P值 0.088 <0.001 <0.001 0.194 <0.001 <0.001 P1值 — <0.001 0.001 — <0.001 <0.001 P2值 — <0.001 <0.001 — <0.001 <0.001 注：血管内皮生长因子（VEGF）、表皮生长因子（EGF）处理因素主效应，F值分别为74.46、76.16,P值均<0.001；时间因素主效应，F值分别为196.95、456.15,P值均<0.001；二者交互作用，F值分别为10.17、10.20,P值均<0.001；t值、P值为组间比较所得，P1值、P2值分别为磷酸盐缓冲液组、脂肪干细胞基质胶组组内各时间点与前一时间点比较所得；“—”表示无此项
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