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五倍子软膏通过调控 mTOR 通路抑制瘢痕疙瘩形成。

Wubeizi Ointment Suppresses Keloid Formation through Modulation of the mTOR Pathway.

机构信息

The First Clinical Medical College, Zhejiang Chinese Medical University, Hangzhou, China.

Department of Dermatology, Xuzhou Hospital Affiliated to Nanjing University of Traditional Chinese Medicine, Xuzhou, China.

出版信息

Biomed Res Int. 2020 Sep 30;2020:3608372. doi: 10.1155/2020/3608372. eCollection 2020.

DOI:10.1155/2020/3608372
PMID:33062677
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7545458/
Abstract

BACKGROUND

Wubeizi ( Mill.) ointment has been shown as an effective treatment for keloids. However, the protective mechanisms of Wubeizi ointment are not fully understood. The mammalian target of rapamycin (mTOR) has been demonstrated to be associated with keloid pathogenesis. In the present study, we investigated if Wubeizi ointment suppressed keloid formation through the modulation of key molecules of the rapamycin (mTOR) pathway including phosphatase and tensin homolog (PTEN), phosphatidylinositol 3-kinase (PI3K), and protein kinase B (Akt).

METHODS

A keloid mouse model and human keloid-derived fibroblasts were developed and treated with Galla chinensis. Immunohistochemistry, western blot, and reverse transcription-PCR were used to detect PI3K, PTEN, Akt, and mTOR in keloid tissues and keloid fibroblasts. The apoptosis and proliferation rate of keloid fibroblasts was, respectively, analyzed by flow cytometry according to the MTT assay. Statistical analysis was done using SPSS version 20.0. For two variable comparisons, a two independent samples -test was used. For multiple variable comparisons, data were analyzed by one-way analysis of variance (ANOVA) followed by pairwise -tests.

RESULTS

Our in vivo and in vitro studies showed that Wubeizi ointment suppressed keloid formation through inhibition of fibroblast proliferation and promotion of fibroblast apoptosis. The underlying basis involves downregulation of p-Akt and p-mTOR as well as upregulation of PTEN.

CONCLUSION

These findings may contribute to a better understanding of the mechanisms of Wubeizi ointment for treating keloids.

摘要

背景

莪术油已被证明是治疗瘢痕疙瘩的有效方法。然而,莪术油的保护机制尚不完全清楚。哺乳动物雷帕霉素靶蛋白(mTOR)已被证明与瘢痕疙瘩的发病机制有关。本研究通过研究莪术油是否通过调节雷帕霉素(mTOR)通路的关键分子,包括磷酸酶和张力蛋白同源物(PTEN)、磷脂酰肌醇 3-激酶(PI3K)和蛋白激酶 B(Akt),来抑制瘢痕疙瘩的形成。

方法

建立瘢痕疙瘩小鼠模型和人瘢痕疙瘩衍生成纤维细胞,并使用莪术油进行处理。免疫组化、western blot 和逆转录-PCR 用于检测瘢痕疙瘩组织和瘢痕疙瘩成纤维细胞中的 PI3K、PTEN、Akt 和 mTOR。根据 MTT 测定法,通过流式细胞术分别分析瘢痕疙瘩成纤维细胞的凋亡和增殖率。使用 SPSS 版本 20.0 进行统计分析。对于两个变量的比较,使用两个独立样本 t 检验。对于多个变量的比较,采用单因素方差分析(ANOVA),然后进行两两比较。

结果

我们的体内和体外研究表明,莪术油通过抑制成纤维细胞增殖和促进成纤维细胞凋亡来抑制瘢痕疙瘩的形成。其潜在基础涉及下调 p-Akt 和 p-mTOR 以及上调 PTEN。

结论

这些发现可能有助于更好地理解莪术油治疗瘢痕疙瘩的机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8ae/7545458/360edf1c93bf/BMRI2020-3608372.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8ae/7545458/9f3654e36360/BMRI2020-3608372.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8ae/7545458/0af65fdd1ea3/BMRI2020-3608372.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8ae/7545458/7e660d31e286/BMRI2020-3608372.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8ae/7545458/61901494918f/BMRI2020-3608372.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8ae/7545458/360edf1c93bf/BMRI2020-3608372.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8ae/7545458/9f3654e36360/BMRI2020-3608372.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8ae/7545458/0af65fdd1ea3/BMRI2020-3608372.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8ae/7545458/7e660d31e286/BMRI2020-3608372.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8ae/7545458/61901494918f/BMRI2020-3608372.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8ae/7545458/360edf1c93bf/BMRI2020-3608372.005.jpg

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