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Hematoporphyrin monomethyl ether-mediated photodynamic therapy inhibits the growth of keloid graft by promoting fibroblast apoptosis and reducing vessel formation.
Photochemical & Photobiological Sciences ( IF 2.7 ) Pub Date : 2020-01-14 , DOI: 10.1039/c9pp00311h
Xiaomei Cui 1 , Jing Zhu 2 , Xiaoyan Wu 1 , Shengju Yang 1 , Xiaodong Yao 1 , Wenyan Zhu 1 , Pan Xu 1 , Xiaodong Chen 1
Affiliation  

Photodynamic therapy (PDT) has been shown to significantly inhibit fibroblast activity. However, the effect of PDT mediated by the photosensitizer hematoporphyrin monomethyl ether (HMME) on keloids is not known well. The aim of our study was to examine the efficacy of HMME-PDT in cellular and animal models of keloids. Keloid fibroblasts (KFbs) were isolated from human keloid specimens and the proliferation, invasion, and migration of KFbs after HMME-PDT treatment was examined in vitro. Apoptosis in cells was measured by flow cytometry. Cysteinyl aspartate specific proteinase 3 (Caspase3) expression was determined by immunofluorescence staining and western blot. HMME-PDT inhibited KFbs proliferation, invasion, migration, increased apoptosis rate and enhanced caspase3 and cleaved caspase3 expression. The keloid graft transplantation was performed by using nude mice. The growth of the graft was monitored every third day. Interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) mRNA expression were detected by quantitative real time PCR. It was observed that HMME-PDT attenuated graft growth and reduced vessel density in the keloid grafts. However, HMME-PDT did not alter IL-6 and TNF-α mRNA expression in the keloid grafts. Moreover, HMME-PDT suppressed transforming growth-β1 (TGF-β1) and small phenotype and Drosophila Mothers Against Decapentaplegic 3 (Smad3) expression in both KFbs and keloid grafts. Collectively, the evidence suggests that HMME-PDT inhibits the growth of the keloid graft by promoting the apoptosis of fibroblasts and reducing vessel formation of the keloid graft.

中文翻译:

血卟啉单甲醚介导的光动力疗法通过促进成纤维细胞凋亡和减少血管形成来抑制瘢痕loid的生长。

光动力疗法(PDT)已显示出显着抑制成纤维细胞活性。然而,由光敏剂血卟啉单甲醚(HMME)介导的PDT对瘢痕loid的作用尚不清楚。我们研究的目的是检查HMME-PDT在瘢痕loid的细胞和动物模型中的功效。从人瘢痕loid标本中分离出瘢痕loid成纤维细胞(KFbs),并在体外检查了HMME-PDT处理后KFbs的增殖,侵袭和迁移。通过流式细胞术测量细胞中的凋亡。通过免疫荧光染色和蛋白质印迹确定半胱氨酸天冬氨酸特异性蛋白酶3(Caspase3)的表达。HMME-PDT抑制KFbs增殖,侵袭,迁移,增加凋亡率并增强caspase3和裂解的caspase3表达。通过使用裸鼠进行瘢痕loid移植。每三天监测一次移植物的生长。实时荧光定量PCR检测白细胞介素6(IL-6)和肿瘤坏死因子-α(TNF-α)mRNA表达。观察到,HMME-PDT减弱了瘢痕s移植物中的移植物生长并降低了血管密度。然而,HMME-PDT不会改变瘢痕loid移植物中的IL-6和TNF-αmRNA表达。此外,HMME-PDT抑制了KFbs和瘢痕loid移植物中的转化生长β1(TGF-β1)和小表型和果蝇母亲对抗Decapentaplegic 3(Smad3)的表达。总体而言,证据表明HMME-PDT通过促进成纤维细胞的凋亡和减少瘢痕loid移植物的血管形成来抑制瘢痕loid移植物的生长。每三天监测一次移植物的生长。实时荧光定量PCR检测白细胞介素6(IL-6)和肿瘤坏死因子-α(TNF-α)mRNA表达。观察到,HMME-PDT减弱了瘢痕s移植物中的移植物生长并降低了血管密度。然而,HMME-PDT不会改变瘢痕loid移植物中的IL-6和TNF-αmRNA表达。此外,HMME-PDT抑制了KFbs和瘢痕loid移植物中的转化生长β1(TGF-β1)和小表型和果蝇母亲对抗Decapentaplegic 3(Smad3)的表达。总体而言,证据表明HMME-PDT通过促进成纤维细胞的凋亡和减少瘢痕loid移植物的血管形成来抑制瘢痕loid移植物的生长。每三天监测一次移植物的生长。实时荧光定量PCR检测白细胞介素6(IL-6)和肿瘤坏死因子-α(TNF-α)mRNA表达。观察到,HMME-PDT减弱了瘢痕s移植物中的移植物生长并降低了血管密度。然而,HMME-PDT不会改变瘢痕loid移植物中的IL-6和TNF-αmRNA表达。此外,HMME-PDT抑制了KFbs和瘢痕loid移植物中的转化生长β1(TGF-β1)和小表型和果蝇母亲对抗Decapentaplegic 3(Smad3)的表达。总体而言,证据表明HMME-PDT通过促进成纤维细胞的凋亡和减少瘢痕loid移植物的血管形成来抑制瘢痕loid移植物的生长。观察到,HMME-PDT减弱了瘢痕s移植物中的移植物生长并降低了血管密度。然而,HMME-PDT不会改变瘢痕loid移植物中的IL-6和TNF-αmRNA表达。此外,HMME-PDT抑制了KFbs和瘢痕loid移植物中的转化生长β1(TGF-β1)和小表型和果蝇母亲对抗Decapentaplegic 3(Smad3)的表达。总体而言,证据表明HMME-PDT通过促进成纤维细胞的凋亡和减少瘢痕loid移植物的血管形成来抑制瘢痕loid移植物的生长。观察到,HMME-PDT减弱了瘢痕s移植物中的移植物生长并降低了血管密度。然而,HMME-PDT不会改变瘢痕loid移植物中的IL-6和TNF-αmRNA表达。此外,HMME-PDT抑制了KFbs和瘢痕loid移植物中的转化生长β1(TGF-β1)和小表型和果蝇母亲对抗Decapentaplegic 3(Smad3)的表达。总体而言,证据表明HMME-PDT通过促进成纤维细胞的凋亡和减少瘢痕loid移植物的血管形成来抑制瘢痕loid移植物的生长。HMME-PDT抑制KFbs和瘢痕loid移植物中的蜕膜生长β1(TGF-β1)和小表型以及果蝇母亲对抗Decapentaplegic 3(Smad3)的表达。总体而言,证据表明HMME-PDT通过促进成纤维细胞的凋亡和减少瘢痕loid移植物的血管形成来抑制瘢痕loid移植物的生长。HMME-PDT抑制KFbs和瘢痕loid移植物中的蜕膜生长β1(TGF-β1)和小表型以及果蝇母亲对抗Decapentaplegic 3(Smad3)的表达。总体而言,证据表明HMME-PDT通过促进成纤维细胞的凋亡和减少瘢痕loid移植物的血管形成来抑制瘢痕loid移植物的生长。
更新日期:2020-02-13
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