Lin Kang, Lü Lei, Gao Wei-Yang, He Zhi-Ling, Zhang Guo-You
Department of Hand and Plastic Surgery, the 2nd Affiliated Hospital of Wenzhou Medical Collge, Wenzhou 325000, China.
Zhonghua Zheng Xing Wai Ke Za Zhi. 2013 Mar;29(2):121-5.
To study the effects of peroxisome proliferator-activated receptor gamma agonists on angiotensin II-induced cellular response in cultured fibroblasts derived from patients with hypertrophic scars, so as to investigate its effects on preventing the formation of hypertrophic scars.
Fibroblasts were freshly isolated from hypertrophic scars and cultured with angiotensin II, rosiglitazone and GW9662 at a certain concentration. Fibroblasts proliferation were assessed via Cell Counting Kit-8; the mRNA and protein expressions of Collagen I and Fibronectin (FN) were determined by quantitative real-time RT-PCR and Western blotting.
The absorbance of CCK-8 and relative expression of Collagen I, FN mRNA and protein were 1.082 5 +/- 0.007, 6.45 +/- 0.97, 4.92 +/- 0.86, 2.92 +/- 0.41, 2.78 +/- 1.04 in Ang II group; 0.722 4 +/- 0.012, 1.82 +/- 0.34, 1.78 +/- 0.27, 1.57 +/- 0.46, 1.68 +/- 0.39 in Ros + Ang II group; 0.554 7 +/- 0.012, 0.97 +/- 0.12, 1.07 +/- 1.08, 1.05 +/- 0.43, 1.14 +/- 0.36 in Ros group; 1.056 0 +/- 0.005, 5.83 +/- 0.24, 4.47 +/- 0.32, 2.69 +/- 0.35, 2.62 +/- 0.27 in GW9662 + ros + Ang II group. The results showed a significant difference between the Ang II group and the control group (P < 0.05). The effect of Ang II could be markedly inhibited by Ros (P < 0.05). In addition, Ros did not influence cell proliferation and production of extracellular matrix (P > 0.05). There was a significant difference between the GW9662 + Ros + Ang II group and the Ros + Ang II (P < 0.05).
PPAR-gamma agonists inhibit Ang II-induced proliferation and extracellular matrix synthesis effectively in the hypertrophic scar fibroblasts. Thus PPAR-gamma agonists may have potential therapeutic effect for hypertrophic scar.
研究过氧化物酶体增殖物激活受体γ激动剂对肥厚性瘢痕患者来源的培养成纤维细胞中血管紧张素Ⅱ诱导的细胞反应的影响，以探讨其对预防肥厚性瘢痕形成的作用。
从肥厚性瘢痕中新鲜分离出成纤维细胞，并用一定浓度的血管紧张素Ⅱ、罗格列酮和GW9662进行培养。通过细胞计数试剂盒-8评估成纤维细胞增殖；采用定量实时逆转录聚合酶链反应和蛋白质印迹法测定Ⅰ型胶原蛋白和纤连蛋白（FN）的mRNA和蛋白质表达。
血管紧张素Ⅱ组CCK-8吸光度及Ⅰ型胶原蛋白、FN mRNA和蛋白质的相对表达分别为1.082 5±0.007、6.45±0.97、4.92±0.86、2.92±0.41、2.78±1.04；罗格列酮+血管紧张素Ⅱ组分别为0.722 4±0.012、1.82±0.34、1.78±0.27、1.57±0.46、1.68±0.39；罗格列酮组分别为0.554 7±0.012、0.97±0.12、1.07±1.08、1.05±0.43、1.14±0.36；GW9662+罗格列酮+血管紧张素Ⅱ组分别为1.056 0±0.005、5.83±0.24、4.47±0.32、2.69±0.35、2.62±0.27。结果显示血管紧张素Ⅱ组与对照组之间有显著差异（P<0.05）。罗格列酮可显著抑制血管紧张素Ⅱ的作用（P<0.05）。此外，罗格列酮不影响细胞增殖和细胞外基质的产生（P>0.05）。GW9662+罗格列酮+血管紧张素Ⅱ组与罗格列酮+血管紧张素Ⅱ组之间有显著差异（P<0.05）。
PPAR-γ激动剂可有效抑制肥厚性瘢痕成纤维细胞中血管紧张素Ⅱ诱导的增殖和细胞外基质合成。因此，PPAR-γ激动剂可能对肥厚性瘢痕具有潜在治疗作用。
