中华整形外科杂志
中華整形外科雜誌
중화정형외과잡지
CHINESE JOURNAL OF PLASTIC SURGERY
2013年
2期
121-125
,共5页
林康%吕雷%高伟阳%何智灵%张国佑
林康%呂雷%高偉暘%何智靈%張國祐
림강%려뢰%고위양%하지령%장국우
增生性瘢痕%过氧化物酶体增殖物激活受体γ%血管紧张素Ⅱ%成纤维细胞
增生性瘢痕%過氧化物酶體增殖物激活受體γ%血管緊張素Ⅱ%成纖維細胞
증생성반흔%과양화물매체증식물격활수체γ%혈관긴장소Ⅱ%성섬유세포
Hypertrophic scar%Peroxisome prolilerator-activated receptor γ%Angiotensin Ⅱ%Fibroblasts
目的 研究过氧化物酶体增殖物激活受体γ(PPAR-γ)激动剂罗格列酮(rosiglitazone,Ros)抑制血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)诱导的人增生性瘢痕成纤维细胞增殖、细胞外基质合成,并探讨其抗瘢痕的潜在作用.方法 体外培养人增生性瘢痕成纤维细胞,在一定浓度的AngⅡ、Ros、GW9662作用下,采用CCK-8法、实时荧光定量RT-PCR和Western blot印迹法分别检测各组成纤维细胞增殖和细胞外基质(ECM)表达的情况.结果 CCK-8法吸光度A值、Ⅰ型胶原蛋白(collagen Ⅰ,Col-Ⅰ)、纤维粘连蛋白(fibronectin,FN) mRNA以及蛋白表达,AngⅡ组分别为1.082 5±0.007、6.45±0.97、4.92±0.86、2.92 +0.41、2.78±1.04；Ros+AngⅡ组为:0.722 4±0.012、1.82±0.34、1.78±0.27、1.57±0.46、t.68 +0.39. Ros组为:0.554 7±0.012、0.97±0.12、1.07±1.08、1.05±0.43、1.14±0.36;GW9662+ Ros+ AngⅡ组为:1.0560±0.005、5.83±0.24、4.47±0.32、2.69±0.35、2.62±0.27.CCK-8法吸光度,Col-Ⅰ和FN mRNA以及蛋白表达量,AngⅡ组与对照组比较,差异有统计学意义(P＜0.05),而Ros+AngⅡ组则使这种效应明显降低(P＜0.05).Ros组和对照组比较,差异无统计学意义(P＞0.05),GW9662+Ros+AngⅡ组与Ros+AngⅡ组比较,差异有统计学意义(P＜0.05).结论 PPAR-γ激动剂可有效抑制AngⅡ诱导的人增生性瘢痕成纤维细胞增殖及Col-Ⅰ和FN合成增多的效应,可能具有体外抗瘢痕纤维化的作用.
目的 研究過氧化物酶體增殖物激活受體γ(PPAR-γ)激動劑囉格列酮(rosiglitazone,Ros)抑製血管緊張素Ⅱ(angiotensinⅡ,AngⅡ)誘導的人增生性瘢痕成纖維細胞增殖、細胞外基質閤成,併探討其抗瘢痕的潛在作用.方法 體外培養人增生性瘢痕成纖維細胞,在一定濃度的AngⅡ、Ros、GW9662作用下,採用CCK-8法、實時熒光定量RT-PCR和Western blot印跡法分彆檢測各組成纖維細胞增殖和細胞外基質(ECM)錶達的情況.結果 CCK-8法吸光度A值、Ⅰ型膠原蛋白(collagen Ⅰ,Col-Ⅰ)、纖維粘連蛋白(fibronectin,FN) mRNA以及蛋白錶達,AngⅡ組分彆為1.082 5±0.007、6.45±0.97、4.92±0.86、2.92 +0.41、2.78±1.04；Ros+AngⅡ組為:0.722 4±0.012、1.82±0.34、1.78±0.27、1.57±0.46、t.68 +0.39. Ros組為:0.554 7±0.012、0.97±0.12、1.07±1.08、1.05±0.43、1.14±0.36;GW9662+ Ros+ AngⅡ組為:1.0560±0.005、5.83±0.24、4.47±0.32、2.69±0.35、2.62±0.27.CCK-8法吸光度,Col-Ⅰ和FN mRNA以及蛋白錶達量,AngⅡ組與對照組比較,差異有統計學意義(P＜0.05),而Ros+AngⅡ組則使這種效應明顯降低(P＜0.05).Ros組和對照組比較,差異無統計學意義(P＞0.05),GW9662+Ros+AngⅡ組與Ros+AngⅡ組比較,差異有統計學意義(P＜0.05).結論 PPAR-γ激動劑可有效抑製AngⅡ誘導的人增生性瘢痕成纖維細胞增殖及Col-Ⅰ和FN閤成增多的效應,可能具有體外抗瘢痕纖維化的作用.
목적 연구과양화물매체증식물격활수체γ(PPAR-γ)격동제라격렬동(rosiglitazone,Ros)억제혈관긴장소Ⅱ(angiotensinⅡ,AngⅡ)유도적인증생성반흔성섬유세포증식、세포외기질합성,병탐토기항반흔적잠재작용.방법 체외배양인증생성반흔성섬유세포,재일정농도적AngⅡ、Ros、GW9662작용하,채용CCK-8법、실시형광정량RT-PCR화Western blot인적법분별검측각조성섬유세포증식화세포외기질(ECM)표체적정황.결과 CCK-8법흡광도A치、Ⅰ형효원단백(collagen Ⅰ,Col-Ⅰ)、섬유점련단백(fibronectin,FN) mRNA이급단백표체,AngⅡ조분별위1.082 5±0.007、6.45±0.97、4.92±0.86、2.92 +0.41、2.78±1.04；Ros+AngⅡ조위:0.722 4±0.012、1.82±0.34、1.78±0.27、1.57±0.46、t.68 +0.39. Ros조위:0.554 7±0.012、0.97±0.12、1.07±1.08、1.05±0.43、1.14±0.36;GW9662+ Ros+ AngⅡ조위:1.0560±0.005、5.83±0.24、4.47±0.32、2.69±0.35、2.62±0.27.CCK-8법흡광도,Col-Ⅰ화FN mRNA이급단백표체량,AngⅡ조여대조조비교,차이유통계학의의(P＜0.05),이Ros+AngⅡ조칙사저충효응명현강저(P＜0.05).Ros조화대조조비교,차이무통계학의의(P＞0.05),GW9662+Ros+AngⅡ조여Ros+AngⅡ조비교,차이유통계학의의(P＜0.05).결론 PPAR-γ격동제가유효억제AngⅡ유도적인증생성반흔성섬유세포증식급Col-Ⅰ화FN합성증다적효응,가능구유체외항반흔섬유화적작용.
Objective To study the effects of peroxisome prolilerator-activated receptor-γ 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.Methods Fibroblasts were freshly isolated from hypertrophic scars and cultured with angioten 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 realtime RT-PCR and Western blotting.Results 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;0.7224±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).Conclusions PPAR-γ agonists inhibit Ang Ⅱ-induced proliferation and extracellular matrix synthesis effectively in the hypertrophic scar fibroblasts.Thus PPAR-γ agonists may have potential therapeutic effect for hypertrophic scar.
