Effects of total flavonoids from<i>Dracocephalum moldavica</i>on the proliferation, migration, and adhesion molecule expression of rat vascular smooth muscle cells induced by TNF-α

Xing, Jianguo; Peng, Kejun; Cao, Wenjiang; Lian, Xuhui; Wang, Qiulin; Wang, Xinchun

doi:10.3109/13880209.2012.711839

Cited by 25 publications

(11 citation statements)

References 28 publications

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“…However, when C5a was added to untreated or C4a-pretreated macrophages and then the supernatant from macrophages was added to VSMCs, it was revealed that C5a-treated macrophages-conditioned medium, which contained cytokines TNF-α, IL-6 and chemokine MCP-1, significantly increased the migration and proliferation of VSMCs, and TNF-α further increased VCAM-1 expression in VSMCs. These results were consistent with previous studies (12,35). The increased migration, proliferation and upregulation of VCAM-1 expression were significantly suppressed when VSMCs were exposed to the conditioned medium from C4a-pretreated macrophages (Fig.…”

Section: Discussionsupporting

confidence: 94%

Complement anaphylatoxin C4a inhibits C5a-induced neointima formation following arterial injury

Zhao

et al. 2014

Molecular Medicine Reports

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Interactions between complement anaphylatoxins have been investigated in numerous fields; however, their functions during arterial remodeling following injury have not been studied. The inhibitory effect of complement anaphylatoxin C4a on neointima formation induced by C5a following arterial injury was investigated. Mice were subjected to wire-induced endothelial denudation of the femoral artery and treated with C5a alone or C5a + C4a for two weeks. C4a significantly inhibited C5a-induced neointima formation and the expression of CD68, F4/80, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and monocyte chemotactic protein-1 (MCP-1). In vitro, although C4a did not directly inhibit the migration, proliferation or the expression of vascular cell adhesion molecule-1 (VCAM-1) of C5a-induced vascular smooth muscle cells (VSMCs), C5a-pretreated conditioned medium-induced migration, proliferation and VCAM-1 expression of VSMCs were suppressed when VSMCs were exposed to conditioned medium from C4a-pretreated macrophages. In addition, C5a-induced TNF-α, IL-6 and MCP-1 expression, Ca2+ influx and extracellular signal-regulated kinase (ERK) activation in macrophages were suppressed by C4a. C4a inhibits C5a-induced neointima formation, not by acting directly on VSMCs, but via a macrophage-mediated reaction by inhibiting the Ca2+-dependent ERK pathway in macrophages.

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Section: Discussionsupporting

confidence: 94%

Complement anaphylatoxin C4a inhibits C5a-induced neointima formation following arterial injury

Zhao

et al. 2014

Molecular Medicine Reports

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“…Disrupting transcription activity of p50-p65 heterodimer, procyanidins decline macrophage-produced IL-6 and COX-2 via blocking LPS-initiated TLR4/NF- κ B pathway [ 99 ]. Ingredients in dracocephalum moldavica normalize the levels of VCAM-1 and ICAM-1 in VSMCs by suppressing TNF- α -triggered NF- κ B signaling [ 100 ]. Moreover, icariin reverses LPS-induced NF- κ B activation and cytokines production in macrophages via boosting PI3K/Akt pathway, whereas saponin glycyrrhizic acid and triterpenoid Ssa restrain inflammation by encumbering PI3K/Akt cascade [ 12 , 101 , 102 ].…”

Section: Mechanisms Of Action Of Chmsmentioning

confidence: 99%

The Signaling Pathways Involved in the Antiatherosclerotic Effects Produced by Chinese Herbal Medicines

Lü

Sun

Qin

et al. 2018

BioMed Research International

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Cardiovascular diseases (CVDs) are considered to be the predominant cause of death in the world. Chinese herb medicines (CHMs) have been widely used for the treatment of CVDs in Asian countries for thousands of years. One reason of high efficacy of CHMs in treating CVDs is attributed to their inhibition in atherosclerosis (AS) development, a critical contributor to CVDs occurrence. Cumulative studies have demonstrated that CHMs alleviate atherogenesis via mediating pathophysiologic events involved in AS. However, there is deficiency in the summaries regarding antiatherogenic signal pathways regulated by CHMs. In this review, we focus on the signal cascades by which herb medicines and relevant extractives, derivatives, and patents improve proatherogenic processes including endothelium dysfunction, lipid accumulation, and inflammation. We mainly elaborate the CHMs-mediated signaling pathways in endothelial cells, macrophages, and vascular smooth muscle cells of each pathogenic event. Moreover, we briefly describe the other AS-related factors such as thrombosis, autophagy, immune response, and noncoding RNAs and effects of CHMs on them in the way of cascade regulation, which is helpful to further illustrate the molecular mechanisms of AS initiation and progression and discover newly effective agents for AS management.

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“…The over-proliferation of VSMCs is one of the key factors in atherosclerosis and the restenosis following percutaneous transcoronary angioplasty (9,10). It has been reported that the flavones and flavonoids extracted from other plants inhibit the proliferation of VSMCs and leiomyomal cells (11,12). Therefore, the present study examined the effects of FDM on the proliferation of VSMCs.…”

Section: Introductionmentioning

confidence: 95%

Effects of total flavones from Dendranthema morifolium on vasocontraction and proliferation of vascular smooth muscle cells

Jin

Liu

Tang

et al. 2015

Molecular Medicine Reports

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Pharmacological studies have shown that the active components in Dendranthema morifolium exhibit protective effects against ischemia/reperfusion injury; however, its pharmacological action on blood vessels has not yet been investigated. The purpose of the present study was to assess the effects of the total flavones extracted from D. morifolium (Ramat.) Tzvel. cv. Hangju (FDM) on the vasocontraction and proliferation of vascular smooth muscle cells (VSMCs). The tension of rat thoracic aortic rings was measured using a mechanical force transducer attached to a recording system. FDM induced a dose‑dependent relaxation of rings with endothelium pre‑contracted by either phenylephrine (PE; 10(‑6) mol/l) or a high concentration of potassium chloride (KCl; 60 mmol/l). FDM did not significantly affect the vasorelaxant effects on mechanically removed endothelium. In endothelium‑denuded aortic rings depolarized by 60 mmol/l KCl, FDM inhibited the contraction induced by Ca2+. FDM reduced the transient contraction caused by PE in a Ca2+‑free solution, but did not affect the contraction induced by phorbol ester. Furthermore, FDM inhibited the proliferation of VSMCs with or without growth stimulation by insulin. In conclusion, that the vasorelaxation induced by FDM in rat aortic rings is not dependent on the endothelium but is mediated via a reduction of the influx of extracellular Ca2+ through the voltage‑dependent and receptor‑operated channels and via the inhibition of the release of intracellular Ca2+ in VSMCs. The anti‑proliferative activity of FDM suggests that it may be beneficial in inhibiting atherosclerosis.

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Effects of total flavonoids fromDracocephalum moldavicaon the proliferation, migration, and adhesion molecule expression of rat vascular smooth muscle cells induced by TNF-α

Abstract: These data suggest that total flavonoids from D. moldavica exhibit anti-inflammatory activities, which is probably one of the underlying mechanisms of D. moldavica for clinical treatment of atherosclerosis.

Cited by 25 publications

References 28 publications

Complement anaphylatoxin C4a inhibits C5a-induced neointima formation following arterial injury

Complement anaphylatoxin C4a inhibits C5a-induced neointima formation following arterial injury

The Signaling Pathways Involved in the Antiatherosclerotic Effects Produced by Chinese Herbal Medicines

Effects of total flavones from Dendranthema morifolium on vasocontraction and proliferation of vascular smooth muscle cells

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