White crystalline powder
Salix babylonicaL.;Salix alba L./Glucoside of poplar and willow bark
Saligenin-β-δ-glucopyranoside/SALICOSIDE/(2R,3S,4S,5R,6S)-2-(Hydroxymethyl)-6-[2-(hydroxymethyl)phenoxy]tetrahydro-2H-pyran-3,4,5-triol/2-(Hydroxymethyl)phenyl β-D-glucopyranoside/Salicyl alcohol-b-glucoside/2-(Hydroxymethyl)phenyl-β-D-glucopyranoside/2-(Hydroxymethyl)phenyl-beta-D-glucopyranoside/(2R,3S,4S,5R,6S)-2-(Hydroxymethyl)-6-[2-(hydroxymethyl)phenoxy]tetrahydro-2H-pyran-3,4,5-triol/Saligenin-β-D-glucopyranoside/(2R,3S,4S,5R,6S)-2-(Hydroxymethyl)-6-(2-(hydroxymethyl)phenoxy)tetrahydro-2H-pyran-3,4,5-triol/Saligenin-b-D-glucopyranoside/o-(Hydroxymethyl)phenyl β-D-glucopyranoside/WHITE WILLOW/Salix alba L./D(-)-Salicin/2-(Hydroxymethyl)phenyl-b-D-glucopyranoside/D-(?)-Salicin/D-(-)-Salicin/β-D-Glucopyranoside, 2-(hydroxymethyl)phenyl/a-Hydroxy-o-tolyl b-D-glucopyranoside/Salicin/Salicine/β-D-Glucopyranoside, 2- (hydroxymethyl)phenyl
Salicin is a natural COX inhibitor.
549.1±50.0 °C at 760 mmHg
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:138-52-3) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Osteoarthritis (OA) is a major age-related disease, which may be caused by the accumulation of advanced glycation end-products (AGEs). Excessive degradation of type II collagen and aggrecan by matrix metalloproteinases (MMPs) and a disintegrin and metalloproteinase with thrombospondin type 1 motif (ADAMTS) induced by AGEs is a pivotal event in the pathogenesis of osteoarthritis. In addition, activation of the nuclear factor-κB (NF-κB) pathway induces the expression of a cascade of proinflammatory cytokines, such as interleukin (IL)-1β and tumor necrosis factor-α (TNF-α). In the present study, we investigated the effects of salicin, one of the main constituents of aspirin and a derivative of Alangium chinense, on AGE-induced degradation of the articular extracellular matrix in SW1353 human chondrocytes. Our findings reveal a novel beneficial role of salicin in rescuing degradation of type II collagen and aggrecan, reducing oxidative stress, attenuating expression of proinflammatory cytokines, and inhibiting activation of the NF-κB proinflammatory signaling pathway in chondrocytes stimulated with AGEs. Salicin may thus have potential as a safe and effective therapy against the development and progression of OA.
Alangium chinense; Osteoarthritis; a disintegrin and metalloproteinase with type 1 thrombospondin motif (ADAMTS); matrix metalloproteinases (MMPs); nuclear factor-κB (NF-κB); salicin.
Salicin Inhibits AGE-induced Degradation of Type II Collagen and Aggrecan in Human SW1353 Chondrocytes: Therapeutic Potential in Osteoarthritis
Feng Gao 1 , Shanyong Zhang 2
Cellular senescence is strongly tied to vascular disease. The current study aims to examine ways that endothelial cellular senescence can be prevented and the mechanisms by which prevention of senescence occurs. Human umbilical vein endothelial cells were exposed to TNF-α to induce senescence; then salicin was administered in two doses – 50 and 100 ?M – to establish a dose-dependent effect of salicin on SA-β-Gal, G1 cell cycle arrest, expression of p21 and PAI-1, p53 acetylation at K382, NRF2 and oxidative stress. NRF2 was examined as a mediating mechanism of salicin’s impact on cellular senescence and was found to account for salicin’s impact on SA-β-Gal, p21, PAI-1 and p53. Together, these results provide a compelling case that salicin has a substantial impact on numerous factors tied to cellular senescence in human endothelial cells. Thus, treatment with salicin may hold promise as a means of preventing aging-related vascular disease. Furthermore, salicin appears to operate via a functional pathway that is different from that affected by anti-inflammatory drugs (e.g. aspirin).
HUVECs; SASP; Salicin; TNF-α; cell senescence; endothelial dysfunction.
Salicin Prevents TNF-α-induced Cellular Senescence in Human Umbilical Vein Endothelial Cells (HUVECs)
Fei Guo 1 , Rong Wu 2 , Jian Xu 1
Retinal endothelial cells (RECs) are involved in many ocular diseases such as age-related macular degeneration (AMD) and diabetic retinopathy. Salicin is the major ingredient of willow bark extract, and it has been shown to be a potent anti-inflammatory agent. We aim to explore whether salicin has a vascular protective effect in RECs. Our data indicate that the presence of salicin in RECs culture media ameliorates interleukin-1β (IL-1β)-induced cellular reactive oxygen species (ROS) production and NADPH oxidase 4 (NOX-4) expression. At the cellular level, salicin attenuates IL-1β-induced mitochondrial injury as revealed by its preservation on mitochondrial membrane potential (MMP). Furthermore, salicin inhibits IL-1β-induced production of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and monocyte chemoattractant protein-1 (MCP-1), vascular adhesion molecules such as intercellular cell adhesion molecule-1 (iCAM-1) and vascular cell adhesion molecule 1 (VCAM-1), and high-mobility group protein 1 (HMGB-1). On the other hand, salicin recovers IL-1β-induced reduction of endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) release. The presence of salicin significantly reduces the IL-1β-induced release of lactate dehydrogenase (LDH), indicating that it mitigates cytokine caused cytotoxicity. Mechanistically, we show that salicin suppresses IL-1β-induced activation of the nuclear factor-kappa B (NF-κB) signaling as revealed by its suppression on nuclear p65 protein and transfected NF-κB promoter. Collectively, our study demonstrates by multiple facets of its mechanisms that salicin is a protective agent in retinal endothelial cells. These results imply its potential use in therapeutic usage of retinal disease.
IL-1β; NF-κB; Retinal endothelial cell (RECs); inflammation; reactive oxygen species (ROS); salicin.
Vascular Protection of Salicin on IL-1β-induced Endothelial Inflammatory Response and Damages in Retinal Endothelial Cells
Yu Song 1 , Xia Tian 1 , Xuehong Wang 1 , Hui Feng 1