2018
DOI: 10.12659/msm.908237
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Emodin, A Chinese Herbal Medicine, Inhibits Reoxygenation-Induced Injury in Cultured Human Aortic Endothelial Cells by Regulating the Peroxisome Proliferator-Activated Receptor-γ (PPAR-γ) and Endothelial Nitric Oxide Synthase (eNOS) Signaling Pathway

Abstract: BackgroundIschemia-reperfusion injury is associated with vascular dysfunction. The aim of this study was to investigate the role of emodin, a Chinese herbal medicine, in hypoxia-reoxygenation injury in cultured human aortic endothelial cells (HAECs) and its effects on the expression of the peroxisome proliferator-activated receptor-γ (PPAR-γ) and endothelial nitric oxide synthase (eNOS) signaling pathway.Material/MethodsAn in vitro hypoxia-reoxygenation model used cultured human aortic endothelial cells (HAECs… Show more

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Cited by 14 publications
(14 citation statements)
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“…Immunomodulation (Wu et al, 2007) TNF-a↓, NF-kB inhibited, caspase-3 inhibited Emodin treatment in BALB/c mice with AMI (Song et al, 2012) TNF-a and IL-1b↓, NF-kBp65 inhibited Emodin treatment in EAM in male Lewis rats (Jiang et al, 2014) IL-1b, IL-6, TNF-a, IL-23, and IL-17↓, NF-kBp65 inhibited Emodin treatment in BALB/c mice with viral myocarditis (Shou et al, 2018) PPAR-g and eNOS phosphorylation↑, NO↑ Emodin treatment in HAECs with ischemia-mimetic (Xu et al, 2018b) BMP2, TRAF1, and RELA↓, calcification, and phenotypical transformation of hVICs via the NF-kB signaling pathway…”
Section: References Finding Methodologymentioning
confidence: 99%
See 1 more Smart Citation
“…Immunomodulation (Wu et al, 2007) TNF-a↓, NF-kB inhibited, caspase-3 inhibited Emodin treatment in BALB/c mice with AMI (Song et al, 2012) TNF-a and IL-1b↓, NF-kBp65 inhibited Emodin treatment in EAM in male Lewis rats (Jiang et al, 2014) IL-1b, IL-6, TNF-a, IL-23, and IL-17↓, NF-kBp65 inhibited Emodin treatment in BALB/c mice with viral myocarditis (Shou et al, 2018) PPAR-g and eNOS phosphorylation↑, NO↑ Emodin treatment in HAECs with ischemia-mimetic (Xu et al, 2018b) BMP2, TRAF1, and RELA↓, calcification, and phenotypical transformation of hVICs via the NF-kB signaling pathway…”
Section: References Finding Methodologymentioning
confidence: 99%
“…In addition, eNOS inhibited the production of inflammatory cytokines by NO dependent mechanisms (Wang et al, 2017). Shou et al (2018) established an in vitro hypoxia-reoxygenation model of human aortic endothelial cells (HAECs). The inactivation of PPAR-g and eNOS signaling pathways is essential for the expression of inflammatory cytokines in endothelial cells induced by hypoxia-reoxygenation.…”
Section: Ppar-g and Enosmentioning
confidence: 99%
“…Phytosterols contained in Aloe gel, such as lonophenol and cycloartenol, are peroxisome proliferator-activated receptor alpha (PPARα) and peroxisome proliferator-activated receptor gamma (PPARγ) agonists in monogastric animals [35], and also emodin is known to activate PPARγ [36]. Although the content of these compounds in our WPH has not been assessed and their effective absorption in blood has never been investigated, most of the effects of Aloe in our transition cows are consistent with the activation of PPAR signaling; these effects are supported by previous results in murine models [17,23,24].…”
Section: Aloe Reduced Mobilization Of Body Reserves and Improved Lipimentioning
confidence: 99%
“…Emodin has been proved to increase the mRNA level of PPARγ and play a protective role in alcohol-mediated liver steatosis [37]. According to the activation of PPARγ signaling pathway, emodin could also alleviate atherosclerosis followed by promoting cholesterol e ux [38], or play other roles though regulating in ammatory response [39,40] and nitric oxide production [41]. Furthermore, emodin has also been reported to regulate the expression of LXRα in atherosclerosis [38] and melanogenesis [42].…”
Section: Discussionmentioning
confidence: 99%