scholarly journals Ten Years’ Research on a Cardiovascular Tonic: A Comprehensive Approach—From Quality Control and Mechanisms of Action to Clinical Trial

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Ping-Chung Leung ◽  
Chi-Man Koon ◽  
Clara Bik-San Lau ◽  
Ping Chook ◽  
William King-Fai Cheng ◽  
...  
Keyword(s):  
Clinical Trials ◽  
Cardiovascular Health ◽  
Foam Cell ◽  
Biological Effects ◽  
Cell Formation ◽  
Surrogate Marker ◽  
Foam Cell Formation ◽  
Herbal Formula ◽  
Interventional Therapies ◽  
Anti Inflammation

Objective. Mortality arising from cardiovascular pathologies remains one of the highest. Maintenance of cardiovascular health therefore remains a universal concern. Interventional therapies and medications have made impressive advances, but preventive measures would be of the same importance.Method. Ten years’ search for a simple herbal formula has resulted in a two-herb combination, consisting ofSalviae Miltiorrhizae Radix et RhizomaandPuerariae Lobatae Radix. The formula has been studied extensively on cardiovascular biological platforms and then put on three clinical trials.Results. In the laboratory, the formula was found to have the biological effects of anti-inflammation, anti-oxidation, anti-foam cell formation on vascular endothelium, and vasodilation. Clinical trials using ultrasonic carotid intima thickness as a surrogate marker showed very significant benefits. No significant adverse effects were encountered.Conclusion. It is therefore recommended that the herbal formula could be used as an adjuvant therapy in cardiac patients under treatment or as a preventive agent among the susceptible.

The Biological Effects of Interleukin-17A on Adhesion Molecules Expression and Foam Cell Formation in Atherosclerotic Lesions

2019 ◽  
Vol 39 (11) ◽  
pp. 694-702 ◽  
Author(s):  
Shohei Shiotsugu ◽  
Toshinori Okinaga ◽  
Manabu Habu ◽  
Daigo Yoshiga ◽  
Izumi Yoshioka ◽  
...  
Keyword(s):  
Adhesion Molecules ◽  
Foam Cell ◽  
Biological Effects ◽  
Cell Formation ◽  
Foam Cell Formation ◽  
Atherosclerotic Lesions ◽  
Interleukin 17A

scholarly journals Study of the interaction of the C-reactive protein monomer with the U937 monocyte

2010 ◽  
Vol 15 (3) ◽  
Author(s):  
Jing Zhao ◽  
Xin-He Shi
Keyword(s):  
Foam Cell ◽  
Biological Effects ◽  
Cell Formation ◽  
Density Lipoprotein ◽  
Surface Proteins ◽  
Foam Cell Formation ◽  
C Reactive Protein ◽  
Monocytic Cell ◽  
Monocytic Cell Line ◽  
Reactive Protein

AbstractC-reactive protein (CRP) has two structurally distinct isoforms, the CRP pentamer and the CRP monomer. A role for the CRP monomer in atherosclerosis is emerging, but the underlying mechanisms are only beginning to be understood. Monocytes are an important contributor to atherosclerosis, and foam cell formation is the hallmark of atherogenesis. However, whether the CRP monomer can directly interact with the monocytes and modulate their responses remains unknown. Furthermore, although FcγRIII (CD16) has been identified as the receptor for the CRP monomer on neutrophils, its role in mediating the CRP monomer’s biological effects in other cell types has been questioned. In this study, we investigated the interaction of the CRP monomer with the monocytes using the U937 monocytic cell line. The CRP monomer specifically binds to U937 cells. This binding is unique in that it is independent of FcγRs and insensitive to protease digestion of the cell surface proteins. Further assays revealed that the CRP monomer directly incorporates into the plasma membrane. Interestingly, the presence of the CRP monomer efficiently retards oxidized low-density lipoprotein-induced foam cell formation of PMA-differentiated U937 macrophages and peripheral blood monocytic cell-derived macrophages. These findings provide additional evidence for the notion that the CRP monomer is an active CRP isoform that plays a role in atherogenesis via the direct modulation of the behavior of the monocytes.

Combating Cardiovascular Disease: Is There a Risk of Foam Cell Formation in Transplanted Angiocompetent Cells Compromising Intended Beneficial Effects of Vascular Regenerative Therapy?.

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 1905-1905
Author(s):  
Eva Rohde ◽  
Elma Aflaki ◽  
Eleonore Froehlich ◽  
Gerhard Lanzer ◽  
Dagmar Kratky ◽  
...  
Keyword(s):  
Clinical Trials ◽  
Smooth Muscle ◽  
Cellular Therapy ◽  
Foam Cell ◽  
Cell Formation ◽  
Nile Red ◽  
Foam Cell Formation ◽  
Regenerative Therapy ◽  
Formation Potential ◽  
Continuous Presence

Abstract Endothelial progenitor cells (EPCs) are the focus of intense clinical research towards vascular regenerative therapy. Somatic vascular EPCs can interact with myelomonocytic and smooth muscle cells modulating the angiogenic response during vascular homeostasis, regeneration and tumour angiogenesis. Interestingly monocytes, either infused freshly after mononuclear cell separation or cultured to induce a pro-angiogenic stimulus prior to re-application, represent the dominant cell fraction in numerous ongoing or already completed clinical trials. Both monocyte-derived macrophages and smooth muscle cells are known to contribute to atherogenesis through lipoprotein endocytosis-mediated foam cell formation. Safety concerns regarding foam cell-related side effects in the course of cellular therapy are evident in atherosclerosis patients. Therefore we examined the foam cell formation potential of typical clinically applied monocyte formulations compared to smooth muscle and endothelial progenitors. Foam cell formation was tested with purified human CD14+ monocytes which were either immediately exposed to 30μg/mL acetylated low-density lipoprotein (acLDL) and cultured for 12 to 72 hours or subjected to a three day pro-angiogenic pre-culture prior to the acLDL exposure. For comparison endothelial colony-forming cells (ECFCs) representing somatic vascular EPCs and multipotent mesenchymal stromal cells (MSCs) as smooth muscle precursors were equally treated in the continuous presence or absence of acLDL. Intracellular lipid accumulation was detected by nile red staining and fluorescence laser scanning microscopy. The number of lipid droplets (LDs) per cell was analyzed using ImageJ software to monitor foam cell formation. Virtual 0.5μm sections were evaluated along the z-axis of a minimum of 40–100 cells per test condition. Depending on cell dimensions, 12 to 30 sections were recorded and LDs were counted in each z-stack. Cellular cholesterol ester and triglyceride content were measured by gas chromatography to further substantiate the pro-atherogenic lipid metabolism. Results revealed intracellular accumulation of bright nile red-fluorescent microvesicles (LDs) in a perinuclear location and size typical for foam cells. Twelve hours of acLDL exposure after a three day pro-angiogenic monocyte pre-culture resulted in a more than three- to 50- fold increased LD count, in comparison to 12h acLDL-exposed fresh monocytes (mean±SD: 42±14; range: 28–58 LDs/cell vs. 5±7; 0–18 LDs/cell; p= 0.027; n=6). Continuous presence of acLDL for 72 hours increased the LD count in cells derived from fresh monocytes two- to 20-fold (20±7; 13–32 LDs/cell; p= 0.046; n=6) but still resulted in decreased numbers of LDs/cell compared to the corresponding pro-angiogenic stimulated monocytes (p=0.046). Surprisingly not only MSCs but also ECFCs displayed foam cell formation potential when subjected to the same permissive conditions in vitro. These data demonstrate that a pro-angiogenic culture can render human monocytes susceptible to foam cell formation. Furthermore, bone marrow-derived MSCs and vascular EPCs also display foam cell formation potential. We speculate that cellular therapy with “foam cell skewed” monocytes and other modified LDL-susceptible candidate regenerative cells may be ineffective or even of risk to patients with cardiovascular diseases, unless underlying pathologic pro-atherogenic conditions are not reverted appropriately. Our data also strengthen requests to re-examine the role that different cell types play during vascular physio-pathology prior to further clinical trials (as exemplified in Blood109:1801; 2007).

Pro–angiogenic Induction of Myeloid Cells for Therapeutic Angiogenesis Can Favor MAPK p38–dependent Foam Cell Formation

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 4442-4442
Author(s):  
Eva Rohde ◽  
Katharina Schallmoser ◽  
Andreas Reinisch ◽  
Nicole A Hofmann ◽  
Thomas Pfeifer ◽  
...  
Keyword(s):  
Clinical Trials ◽  
Progenitor Cells ◽  
Foam Cell ◽  
Cell Formation ◽  
Hematopoietic Cells ◽  
Cell Types ◽  
Foam Cells ◽  
Therapeutic Angiogenesis ◽  
Foam Cell Formation ◽  
Vascular Regeneration

Abstract Abstract 4442 Background: Clinical trials for therapeutic angiogenesis use blood- or marrow-derived transplants containing hematopoietic cells, endothelial progenitor cells (EPCs) and mesenchymal stem and progenitor cells (MSPCs) to support vascular regeneration. Recently concerns have emerged, as bone marrow-derived stem cell preparations also include these three cell types which probably may contribute to atherosclerosis. We therefore asked whether human myelomonocytic hematopoietic cells, EPCs or MSPCs after pro-angiogenic induction can accumulate lipid droplets (LDs) and develop into foam cells. Method: LD accumulation was quantified by flow cytometry, confocal microscopy and cholesterol measurement in each of the tested cell types. The impact of an initial three-day pro-angiogenic culture on subsequent foam cell formation was studied to mimic a relevant setting already being used in clinical trials. The phosphorylation state of intracellular signaling molecules in response to pro-angiogenic stimulation was determined to delineate the operative mechanisms and to establish a basis for interventional strategies. Result: Foam cells were formed by monocytes but neither by EPCs nor by MSPCs after pro-angiogenic induction. Mitogen-activated protein kinase (MAPK) p38 phosphorylation was enhanced in monocytes after pro-angiogenic stimulation. Kinase inhibition almost abrogated intracellular LD accumulation. Conclusion: These data suggest that hematopoietic cell preparations containing monocytes bear the risk of foam cell formation after pro-angiogenic induction. EPCs and MSPCs instead may drive vascular regeneration without atherogenesis aggravation. A thorough understanding of cell biology is necessary to develop new strategies combining pro-angiogenic and anti-atherogenic cellular effects during therapeutic angiogenesis. Disclosures: No relevant conflicts of interest to declare.

EM of human atherosclerosis: Aortic fatty streaks with transitional lesion features

1992 ◽  
Vol 50 (1) ◽  
pp. 622-623
Author(s):  
K. Florian Klemp ◽  
J.R. Guyton
Keyword(s):  
Foam Cell ◽  
Cell Formation ◽  
Processing Technique ◽  
Foam Cell Formation ◽  
Tissue Preparation ◽  
Electron Microscopic ◽  
Extracellular Lipid ◽  
Electron Microscopic Cytochemistry ◽  
Human Atherosclerosis ◽  
Clinically Significant

The earliest distinctive lesions in human atherosclerosis are fatty streaks (FS), characterized initially by lipid-laden foam cell formation. Fibrous plaques (FP), the clinically significant lesions, differ from FS in several respects. In addition to foam cells, the FP also exhibit fibromuscular proliferation and a necrotic core region rich in extracellular lipid. The possible transition of FS into mature FP has long been debated, however. A subset of FS described by Katz etal., was intermediate in lipid composition between ordinary FS and FP. We investigated this hypothesis by electron microscopic cytochemistry by employing a tissue processing technique previously described by our laboratory. Osmium-tannic acid-paraphenylenediamine (OTAP) tissue preparation enabled ultrastructural analysis of lipid deposits to discern features characteristic of mature fibrous plaques.

Aged Garlic Extract Inhibits CD36 Expression and Foam Cell Formation in Human Macrophages

Planta Medica ◽  
2007 ◽  
Vol 73 (09) ◽  
Author(s):  
N Ide ◽  
N Morihara ◽  
L Paptheodorou ◽  
R Stirner ◽  
N Weiss
Keyword(s):  
Foam Cell ◽  
Cell Formation ◽  
Garlic Extract ◽  
Foam Cell Formation ◽  
Aged Garlic Extract ◽  
Human Macrophages ◽  
Cd36 Expression ◽  
Aged Garlic

Dynamic Role of Macrophage Sub Types for Development of Atherosclerosis and Potential Use of Herbal Immunomodulators as Imminent Therapeutic Strategy

2020 ◽  
Vol 18 ◽  
Author(s):  
Parimalanandhini Duraisamy ◽  
Sangeetha Ravi ◽  
Mahalakshmi Krishnan ◽  
Catherene M. Livya ◽  
Beulaja Manikandan ◽  
...  
Keyword(s):  
Foam Cell ◽  
Cell Formation ◽  
Atherosclerotic Lesion ◽  
Foam Cell Formation ◽  
Atherosclerosis Progression ◽  
Proinflammatory Mediators ◽  
M1 Macrophage ◽  
Tnf Α ◽  
Inflammatory Site

: Atherosclerosis, a major contributor to cardiovascular disease is a global alarm causing mortality worldwide. Being a progressive disease in the arteries, it mainly causes recruitment of monocytes to the inflammatory sites and subside pathological conditions. Monocyte-derived macrophage mainly acts in foam cell formation by engorging the LDL molecules, oxidizes it into Ox-LDL and leads to plaque deposit development. Macrophages in general differentiate, proliferate and undergo apoptosis at the inflammatory site. Frequently two subtypes of macrophages M1 and M2 has to act crucially in balancing the micro-environmental conditions of endothelial cells in arteries. The productions of proinflammatory mediators like IL-1, IL-6, TNF-α by M1 macrophage has atherogenic properties majorly produced during the early progression of atherosclerotic plaques. To counteract cytokine productions and M1-M2 balance, secondary metabolites (phytochemicals) from plants act as a therapeutic agent in alleviating atherosclerosis progression. This review summarizes the fundamental role of the macrophage in atherosclerotic lesion formation along with its plasticity characteristic as well as recent therapeutic strategies using herbal components and anti-inflammatory cytokines as potential immunomodulators.

ClC-3: A Novel Promising Therapeutic Target for Atherosclerosis

2021 ◽  
pp. 107424842110236
Author(s):  
Dun Niu ◽  
Lanfang Li ◽  
Zhizhong Xie
Keyword(s):  
Therapeutic Target ◽  
Chloride Channels ◽  
Foam Cell ◽  
Low Density Lipoprotein ◽  
Cell Formation ◽  
Density Lipoprotein ◽  
Molecular Structures ◽  
Foam Cell Formation ◽  
Endothelium Dysfunction ◽  
Atherosclerotic Process

Chloride channel 3 (ClC-3), a Cl−/H+ antiporter, has been well established as a member of volume-regulated chloride channels (VRCCs). ClC-3 may be a crucial mediator for activating inflammation-associated signaling pathways by regulating protein phosphorylation. A growing number of studies have indicated that ClC-3 overexpression plays a crucial role in mediating increased plasma low-density lipoprotein levels, vascular endothelium dysfunction, pro-inflammatory activation of macrophages, hyper-proliferation and hyper-migration of vascular smooth muscle cells (VSMCs), as well as oxidative stress and foam cell formation, which are the main factors responsible for atherosclerotic plaque formation in the arterial wall. In the present review, we summarize the molecular structures and classical functions of ClC-3. We further discuss its emerging role in the atherosclerotic process. In conclusion, we explore the potential role of ClC-3 as a therapeutic target for atherosclerosis.

scholarly journals Protective Effect of Lusianthridin on Hemin-Induced Low-Density Lipoprotein Oxidation

2021 ◽  
Vol 14 (6) ◽  
pp. 567
Author(s):  
Su Wutyi Thant ◽  
Noppawan Phumala Morales ◽  
Visarut Buranasudja ◽  
Boonchoo Sritularak ◽  
Rataya Luechapudiporn
Keyword(s):  
Foam Cell ◽  
Low Density Lipoprotein ◽  
Cell Formation ◽  
Density Lipoprotein ◽  
Foam Cell Formation ◽  
Raw 264.7 ◽  
Low Density ◽  
Lipoprotein Oxidation ◽  
Raw 264.7 Macrophage Cells ◽  
Low Density Lipoprotein Oxidation

Oxidation of low-density lipoprotein (LDL) plays a crucial role in the pathogenesis of atherosclerosis. Hemin (iron (III)-protoporphyrin IX) is a degradation product of hemoglobin that can be found in thalassemia patients. Hemin is a strong oxidant that can cause LDL oxidation and contributes to atherosclerosis in thalassemia patients. Lusianthridin from Dendrobium venustrum is a phenolic compound that possesses antioxidant activity. Hence, lusianthridin could be a promising compound to be used against hemin-induced oxidative stress. The major goal of this study is to evaluate the protective effect of lusianthridin on hemin-induced low-density lipoprotein oxidation (he-oxLDL). Here, various concentrations of lusianthridin (0.25, 0.5, 1, and 2 µM) were preincubated with LDL for 30 min, then 5 µM of hemin was added to initiate the oxidation, and oxidative parameters were measured at various times of incubation (0, 1, 3, 6, 12, 24 h). Lipid peroxidation of LDL was measured by thiobarbituric reactive substance (TBARs) assay and relative electrophoretic mobility (REM). The lipid composition of LDL was analyzed by using reverse-phase HPLC. Foam cell formation with he-oxLDL in RAW 264.7 macrophage cells was detected by Oil Red O staining. The results indicated that lusianthridin could inhibit TBARs formation, decrease REM, decrease oxidized lipid products, as well as preserve the level of cholesteryl arachidonate and cholesteryl linoleate. Moreover, He-oxLDL incubated with lusianthridin for 24 h can reduce the foam cell formation in RAW 264.7 macrophage cells. Taken together, lusianthridin could be a potential agent to be used to prevent atherosclerosis in thalassemia patients.

Sign in / Sign up

Export Citation Format

Share Document