[Aloe-emodin inhibits scar tissue fibrosis through thrombospondin-1-PI3k-Akt pathway].

Hongbao Geng, Xingyi Zhang, Siwei Zhou, Na Li, Jia Liu, Xuewei Yuan, Chunliu Ning, Xudong Zhang, Wei Huang
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引用次数: 0

Abstract

Objectives: To propose a hypothesis that aloe-emodin may inhibit scar tissue fibrosis through thrombospondin-1(THBS1)-PI3K-Akt pathway.

Methods: By cultivating fibroblasts derived from scar tissue after cleft palate surgery in humans, aloe emodin of different concentrations (10, 20, 30, 40 and 50 μmol/L) was added to the cells which activity was detected. At the same time, transcriptome sequencing was performed on scar tissue and cells, and bioinformatics methods were used to explore potential targets and signaling pathways of scar tissue fibrosis.

Results: Aloe-emodin had a concentration dependent inhibitory effect on fibroblast proliferation,with the 40 μmol/L concentration group showing the most significant effect. The results of tissue and cell sequencing indicated that differentially expressed genes were significantly enriched in extracellular matrix-receptor interaction pathway, and shared a common differential gene which was THBS1. The ORA analysis results indicated that differentially expressed genes, including THBS1, were significantly enriched in the PI3K-Akt signaling pathway.

Conclusions: Aloe emodin may inhibit the PI3K-Akt pathway by downregulating THBS1, thereby reducing the proliferation activity of fibroblasts derived from postoperative palatal scar tissue.

[芦荟大黄素通过血栓反应蛋白-1- pi3k - akt通路抑制疤痕组织纤维化]。
目的:提出芦荟大黄素可能通过血栓反应蛋白-1(THBS1)-PI3K-Akt通路抑制疤痕组织纤维化的假说。方法:通过培养人腭裂术后瘢痕组织成纤维细胞,分别加入不同浓度(10、20、30、40、50 μmol/L)的芦荟大黄素,检测细胞活性。同时,对疤痕组织和细胞进行转录组测序,并利用生物信息学方法探索疤痕组织纤维化的潜在靶点和信号通路。结果:芦荟大黄素对成纤维细胞增殖的抑制作用具有浓度依赖性,以40 μmol/L浓度组效果最显著。组织和细胞测序结果表明,细胞外基质-受体相互作用通路差异表达基因显著富集,并共享一个共同的差异基因THBS1。ORA分析结果显示,包括THBS1在内的差异表达基因在PI3K-Akt信号通路中显著富集。结论:芦荟大黄素可能通过下调THBS1抑制PI3K-Akt通路,从而降低术后腭瘢痕组织成纤维细胞的增殖活性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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