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aesculin/inflammation
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6 results
Aesculin modulates bone metabolism by suppressing receptor activator of NF-κB ligand (RANKL)-induced osteoclastogenesis and transduction signals.
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Aesculin (AES), a coumarin compound derived from Aesculus hippocasanum L, is reported to exert protective role against inflammatory diseases, gastric disease and cancer. However, direct effect of AES in bone metabolism is deficient. In this study, we examined the effects of AES on osteoclast (OC)
Glycosylation enables aesculin to activate Nrf2.
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Since aesculin, 6,7-dihydroxycoumarin-6-O-β-glucopyranoside, suppresses inflammation, we asked whether its anti-inflammatory activity is associated with the activation of nuclear factor-E2-related factor 2 (Nrf2), a key anti-inflammatory factor. Our results, however, show that aesculin marginally
Aesculin inhibits matrix metalloproteinase-9 expression via p38 mitogen activated protein kinase and activator protein 1 in lipopolysachride-induced RAW264.7 cells.
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Expression of matrix metalloproteinase 9 (MMP-9) may contribute to inflammatory conditions such as arthritis, hepatitis, atherosclerosis, and pulmonary fibrosis, which involves the destruction of the extracellular matrix (ECM). Macrophages stimulated with lipopolysaccharide (LPS) express MMP-9
Aesculin protects against DSS-Induced colitis though activating PPARγ and inhibiting NF-кB pathway.
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Aesculin, a natural product from the traditional and widely-used Chinese medicine named Cortex fraxini, has attracted attention as a novel therapeutic modulator of inflammation. However, little is known about its effect on ulcerative colitis (UC). This study aimed to investigate the protective
Chinese herbal medicinal ingredients inhibit secretion of IL-6, IL-8, E-selectin and TXB2 in LPS-induced rat intestinal microvascular endothelial cells.
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The aim of the research was to investigate the anti-inflammatory mechanism of Pulsatillae Decoction (PD), the levels of interleukin (IL)-6, IL-8, E-selectin, and thromboxane B(2) (TXB(2)) secreted by cultured rat intestinal microvascular endothelial cells (RIMECs) were determined after treatment
Pulsatilla decoction and its active ingredients inhibit secretion of NO, ET-1, TNF-alpha, and IL-1 alpha in LPS-induced rat intestinal microvascular endothelial cells.
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To investigate the pharmacological mechanism of the traditional Chinese medicine, Pulsatilla decoction (PD), the levels of nitric oxide (NO), endothelin-1 (ET-1), tumor necrosis factor-alpha (TNF-alpha), and interleukin-1 alpha (IL-1 alpha) secreted by cultured rat intestinal microvascular
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