scholarly journals Mitochondrion-Targeted Peptide SS-31 Inhibited Oxidized Low-Density Lipoproteins-Induced Foam Cell Formation through both ROS Scavenging and Inhibition of Cholesterol Influx in RAW264.7 Cells

Molecules ◽  
2015 ◽  
Vol 20 (12) ◽  
pp. 21287-21297 ◽  
Author(s):  
Shuangying Hao ◽  
Jiajie Ji ◽  
Hongting Zhao ◽  
Longcheng Shang ◽  
Jing Wu ◽  
...  
2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Johnna Francis Varghese ◽  
Rohit Patel ◽  
Mohit Singh ◽  
Umesh Chand Singh Yadav

Cell Reports ◽  
2016 ◽  
Vol 14 (12) ◽  
pp. 2859-2871 ◽  
Author(s):  
Harikesh S. Wong ◽  
Valentin Jaumouillé ◽  
Spencer A. Freeman ◽  
Sasha A. Doodnauth ◽  
Daniel Schlam ◽  
...  

1995 ◽  
Vol 114 (1) ◽  
pp. 123-132 ◽  
Author(s):  
Takeshi Nishikawa ◽  
Shozo Kobori ◽  
Haruo Takeda ◽  
Takayuki Higashi ◽  
Yoshihiro Sato ◽  
...  

2021 ◽  
Vol 14 (6) ◽  
pp. 567
Author(s):  
Su Wutyi Thant ◽  
Noppawan Phumala Morales ◽  
Visarut Buranasudja ◽  
Boonchoo Sritularak ◽  
Rataya Luechapudiporn

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.


2012 ◽  
Vol 65 (9-10) ◽  
pp. 388-395 ◽  
Author(s):  
Danijela Vucevic ◽  
Djordje Radak ◽  
Tatjana Radosavljevic ◽  
Dusan Mladenovic ◽  
Ivan Milovanovic

Introduction. Atherosclerosis is a progressive, multifactorial, diffuse, multisystemic, chronic, inflammatory disease, which is manifested by disorders of vascular, immune and metabolic system. Pathogenesis of this disease is not fully understood. Endothelial Dysfunction and Inflammatory Process. Endothelial dysfunction is recognized as the crucial step in atherogenesis. A lot of studies have confirmed the involvement of various mediators of inflammation in initial proatherogenic processes, such as the upregulation of adhesion molecules on endothelial cells, binding of low density lipoproteins to endothelium, activation of macrophages and proliferation of vascular smooth muscle cells. Fatty stain and Inflammatory Process. Fatty stain consists of foam cell accumulation. After foam cell formation, mediators of inflammation initiate a series of intracellular events that include the induction of inflammatory cytokines. Thus, a vicious circle of inflammation, modification of lipoproteins and further inflammation can be maintained in the artery. Transitory Lesion and Inflammatory Process. In transitory lesion intensive phagocytosis of oxidized low density lipoproteins additionally activates monocytes and macrophages and consequently facilitates and exacerbates the inflammatory response. Fibrotic Plaque and Inflammatory Process. Inflammatory process, matrix-degrading metalloproteinases activity, platelets aggregation and smooth muscle cells proliferation play a central role in development of fibrotic plaque. Complex Lesion and Inflammatory Process. It has been shown that inflammation is closely related to the development of atherosclerotic plaque rupture. Conclusion. The contribution of inflammatory process has become increasingly meaningful in understanding the initiation, progression and clinical manifestations of atherosclerosis.


1988 ◽  
Vol 16 (6) ◽  
pp. 877-879
Author(s):  
Kenji ISHII ◽  
Toru KITA ◽  
Yutaka NAGANO ◽  
Noriaki KUME ◽  
Masayuki YOKODE ◽  
...  

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