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补中逐瘀汤(CTJ)通过细胞骨架重塑途径抑制血管平滑肌细胞的粘附和迁移。

Chungtaejeon (CTJ) inhibits adhesion and migration of VSMC through cytoskeletal remodeling pathway.

作者信息

Paudel Keshav Raj, Panth Nisha, Kim Dong Wook, Karki Rajendra

机构信息

Department of Oriental Medicine Resource, Mokpo National University, Muan-gun, Jeonnam, 58554, Republic of Korea.

College of Pharmacy and Natural Medicine Research Institute, Mokpo National University, Muan-gun, Jeonnam, 58554, Republic of Korea.

出版信息

Heliyon. 2024 Sep 26;10(19):e38508. doi: 10.1016/j.heliyon.2024.e38508. eCollection 2024 Oct 15.

DOI:10.1016/j.heliyon.2024.e38508
PMID:39397925
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11471206/
Abstract

INTRODUCTION

Vascular remodeling is crucial for the progression of vascular disease such as atherosclerosis. We utilize the experimental model of atherosclerosis to elucidate the activity of Chungtaejeon (CTJ), a Korean fermented tea on adhesion and migration of human aortic vascular smooth muscle cells (HASMC).

MATERIALS AND METHODS

Various assays such as cell viability, cell adhesion, Western blot, immunofluorescence, were carried out on HASMC to explore pathway associated with cytoskeletal remodeling during the progression of atherosclerosis.

RESULTS

In result, CTJ significantly inhibited adhesion of HASMC as revealed by collagen assay. Similarly, CTJ inhibited the β1-integrin protein expression as well as FAK phosphorylation. Treatment of CTJ also inhibited stress fiber formation. Likewise, adherence of cells on collagen optimally increased the expression of both RhoA and Cdc42, however, treatment of CTJ dose dependently decreased their expression. The lysophosphatidic acid stimulation of HASMC rapidly increased the level of phosphorylated forms of MLC20 within 15 min, followed by an extended level of MLC20 phosphorylation. The treatment of CTJ at a dose of 50, 100 and 250 μg/ml remarkably reduced the diphosphorylated form while decreased the level of monophosphorylated form of MLC20.

CONCLUSIONS

Our results suggests that, with further validation CTJ could be a promising herbal resource for prevention of atherosclerosis.

摘要

引言

血管重塑对于动脉粥样硬化等血管疾病的进展至关重要。我们利用动脉粥样硬化实验模型来阐明韩国发酵茶Chungtaejeon(CTJ)对人主动脉血管平滑肌细胞(HASMC)黏附和迁移的作用。

材料与方法

对HASMC进行了多种检测,如细胞活力、细胞黏附、蛋白质印迹法、免疫荧光法,以探索动脉粥样硬化进展过程中与细胞骨架重塑相关的途径。

结果

结果显示,胶原蛋白检测表明CTJ显著抑制HASMC的黏附。同样,CTJ抑制β1整合素蛋白表达以及黏着斑激酶磷酸化。CTJ处理还抑制应力纤维形成。同样,细胞在胶原蛋白上的黏附最佳地增加了RhoA和Cdc42的表达,然而,CTJ处理剂量依赖性地降低了它们的表达。溶血磷脂酸刺激HASMC在15分钟内迅速增加MLC20磷酸化形式的水平,随后MLC20磷酸化水平持续升高。50、100和250μg/ml剂量的CTJ处理显著降低了MLC20的双磷酸化形式,同时降低了单磷酸化形式的水平。

结论

我们的结果表明,经过进一步验证,CTJ可能是一种有前景的预防动脉粥样硬化的草药资源。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f63/11471206/dca112c3e5a3/mmcfigs6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f63/11471206/aa64c1bb8cea/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f63/11471206/7ef00fce38ce/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f63/11471206/611b9ac6a0cd/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f63/11471206/6614ad940450/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f63/11471206/24b034e780a4/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f63/11471206/becc2587a57e/mmcfigs1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f63/11471206/3c47b7581855/mmcfigs2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f63/11471206/9cb15b53a4ed/mmcfigs3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f63/11471206/67dd2f22807b/mmcfigs4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f63/11471206/224cb345a8fe/mmcfigs5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f63/11471206/dca112c3e5a3/mmcfigs6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f63/11471206/aa64c1bb8cea/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f63/11471206/7ef00fce38ce/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f63/11471206/611b9ac6a0cd/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f63/11471206/6614ad940450/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f63/11471206/24b034e780a4/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f63/11471206/becc2587a57e/mmcfigs1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f63/11471206/3c47b7581855/mmcfigs2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f63/11471206/9cb15b53a4ed/mmcfigs3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f63/11471206/67dd2f22807b/mmcfigs4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f63/11471206/224cb345a8fe/mmcfigs5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f63/11471206/dca112c3e5a3/mmcfigs6.jpg

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