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大黄素对机械应力诱导的增生性瘢痕炎症的抑制作用

Inhibition of mechanical stress-induced hypertrophic scar inflammation by emodin.

作者信息

Liu Cheng

机构信息

Department of Plastic Surgery, Jiangxi Provinicial People's Hospital, Nanchang, Jiangxi 330006, P.R. China.

出版信息

Mol Med Rep. 2015 Jun;11(6):4087-92. doi: 10.3892/mmr.2015.3265. Epub 2015 Jan 28.

DOI:10.3892/mmr.2015.3265
PMID:25634255
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4394962/
Abstract

At least 50% of hypertrophic scarring (HS) is characterized by inflammation, for which there is currently no effective treatment available. Emodin is a major component of the widely used Chinese herb, rhubarb, which has been used to treat inflammation in several types of disease. However, few studies have investigated the efficacy of emodin in the treatment of HS. In the present study, a mouse model with mechanical stress‑induced HS was used to investigate the effects of emodin (20, 40, 80, or 120 mg/ml) on HS, and to determine the potential underlying mechanisms. Treatment with emodin significantly attenuated HS inflammation, as determined by histopathological assessment of the scar elevation index, collagen structure and inflammation (P<0.05). Furthermore, treatment with emodin (40 mg/ml) markedly inhibited phosphoinositide 3‑kinase (PI3K)/Akt activity (P<0.01) and this attenuation was associated with reduced expression levels of tumor necrosis factor‑α, interleukin‑6 and monocyte chemoattractant protein‑1 (P<0.05) in the HS tissue. The results of the present study indicated that administration of emodin had therapeutic effects on the progression of HS and the underlying mechanism of this may be due to inhibition of the PI3K/Akt signaling pathway.

摘要

至少50%的增生性瘢痕(HS)以炎症为特征,目前尚无有效的治疗方法。大黄素是广泛使用的中药大黄的主要成分,已被用于治疗多种疾病的炎症。然而,很少有研究调查大黄素治疗HS的疗效。在本研究中,使用机械应力诱导HS的小鼠模型来研究大黄素(20、40、80或120mg/ml)对HS的影响,并确定潜在的作用机制。通过对瘢痕隆起指数、胶原结构和炎症的组织病理学评估确定,大黄素治疗显著减轻了HS炎症(P<0.05)。此外,大黄素(40mg/ml)治疗显著抑制了磷酸肌醇3激酶(PI3K)/Akt活性(P<0.01),这种减轻与HS组织中肿瘤坏死因子-α、白细胞介素-6和单核细胞趋化蛋白-1表达水平降低有关(P<0.05)。本研究结果表明,大黄素给药对HS进展具有治疗作用,其潜在机制可能是抑制PI3K/Akt信号通路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/4394962/c48da2da0148/MMR-11-06-4087-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/4394962/a58ed5683d1e/MMR-11-06-4087-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/4394962/0390233e4a7e/MMR-11-06-4087-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/4394962/61e91759db1e/MMR-11-06-4087-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/4394962/55a498fd38a5/MMR-11-06-4087-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/4394962/cbe7244242d0/MMR-11-06-4087-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/4394962/c48da2da0148/MMR-11-06-4087-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/4394962/a58ed5683d1e/MMR-11-06-4087-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/4394962/0390233e4a7e/MMR-11-06-4087-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/4394962/61e91759db1e/MMR-11-06-4087-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/4394962/55a498fd38a5/MMR-11-06-4087-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/4394962/cbe7244242d0/MMR-11-06-4087-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/4394962/c48da2da0148/MMR-11-06-4087-g05.jpg

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