Salidroside Inhibits Lipopolysaccharide-ethanol-induced Activation of Proinflammatory Macrophages via Notch Signaling Pathway

Li, Jian-Sha; Fan, Lu-Yao; Yuan, Meng-Dan; Xing, Mingyou

doi:10.1007/s11596-019-2069-4

Cited by 22 publications

(14 citation statements)

References 38 publications

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“…24 Other studies showed shown that salidroside significantly inhibited NF-κB phosphorylation in a dose-dependent manner via the Notch/HES signaling pathway, and also blocked extracellular signal-regulated kinase/mitogen-activated protein kinase, thereby reducing the secretion of TNF-α, IL-6, and IL-1β, significantly reducing the infiltration and inflammatory exudation of lung neutrophils, reducing pulmonary edema and increasing the survival of septic mice; it also exerted anti-infection and protective effects against ALI caused by sepsis in mice. 25,26 Studies showed that salidroside could also ameliorate alcohol-induced hepatitis damage by regulating the inflammatory response of macrophages. 27 In a study of ALI caused by LPS, Sal significantly reduced the activity of pro-inflammatory factors TNF-α, IL-6, and IL-1β in lung tissue homogenates by inhibiting the TLR /NF-κB pathway.…”

Section: Discussionmentioning

confidence: 99%

Mechanism and Experimental Verification of the Use of Rhodiola crenulata to Cytokine Storm Based on Network Pharmacology and Molecular Docking

Zhao

Song

Wang

et al. 2022

Natural Product Communications

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Objective: To identify the potential biological mechanisms by which Rhodiola crenulata (RC) treats cytokine storm (CS) using network pharmacology, molecular docking, and experimental verification. Methods: The ingredients and targets of RC were collected from the Organchem database. CS-related genes were collected using the GeneCards and OMIM databases. Cytoscape 3.7.2 software was used to construct the RC-CS network diagram. These data were inputted into the STRING database to construct a protein–protein interaction network. we performed gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes enrichment analysis using DAVID and R software. Molecular docking of the active ingredient and pathway-related targets was carried out using AutoDock Vina and PyMOL, and then a CS model was established in rats induced by lipopolysaccharide for in vivo experimental verification. Results: The network pharmacology results showed that kaempferol was the most important active component of RC in the treatment of CS, and IL6 and STAT3 were identified as key targets. Molecular docking results showed that RC active components kaempferol had a good binding ability to IL6/STAT3. At the same time, compared with the model group, different doses of kaempferol could down-regulate the expression of inflammatory factors ( P < .05), and protect against systemic inflammatory response multiple organ damage. Conclusion: This study preliminarily revealed that RC can prevent and treat CS by regulating the expression of inflammatory factors, inhibiting the systemic inflammatory response induced by lipopolysaccharide, and providing a theoretical basis for the study of its pharmacodynamic material basis and mechanism of action.

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Section: Discussionmentioning

confidence: 99%

Mechanism and Experimental Verification of the Use of Rhodiola crenulata to Cytokine Storm Based on Network Pharmacology and Molecular Docking

Zhao

Song

Wang

et al. 2022

Natural Product Communications

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“…At present, it is generally believed that TNF-α and IL-1β, the "early" pro-inflammatory mediators, are the key inflammatory factors causing uncontrolled inflammatory response and tissue damage [22,23] . Recent studies have shown that HMGB1 is a key "late" proinflammatory mediator, which plays an important role in sepsis.…”

Section: Discussionmentioning

confidence: 99%

Nucleolin Mediates LPS-induced Expression of Inflammatory Mediators and Activation of Signaling Pathways

Wang

Huang

et al. 2020

CURR MED SCI

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In this study, we investigated the effects of nucleolin on lipopolysaccharide (LPS)induced activation of MAPK and NF-KappaB (NF-κB) signaling pathways and secretion of TNF-α, IL-1β and HMGB1 in THP-1 monocytes. Immunofluorescence assay and Western blotting were used to identify the nucleolin expression in cell membrane, cytoplasm and nucleus of THP-1 monocytes. Inactivation of nucleolin was induced by neutralizing antibody against nucleolin. THP-1 monocytes were pretreated with anti-nucleolin antibody for 1 h prior to LPS challenge. The irrelevant IgG group was used as control. Secretion of inflammatory mediators (TNF-α, IL-1β and HMGB1) and activation of MAPK and NF-κB/I-κB signaling pathways were examined to assess the effects of nucleolin on LPS-mediated inflammatory response. Nucleolin existed in cell membrane, cytoplasm and nucleus of THP-1 monocytes. Pretreatment of anti-nucleolin antibody significantly inhibited the LPS-induced secretion of TNF-α, IL-1β and HMGB1. P38, JNK, ERK and NF-κB subunit p65 inhibitors could significantly inhibit the secretion of IL-1β, TNF-α and HMGB1 induced by LPS. Moreover, the phosphorylation of p38, JNK, ERK and p65 (or nuclear translocation of p65) was significantly increased after LPS challenge. In contrast, pretreatment of anti-nucleolin antibody could significantly inhibit the LPS-induced phosphorylation of p38, JNK, ERK and p65 (or nuclear translocation of p65). However, the irrelevant IgG, as a negative control, had no effect on LPS-induced secretion of TNF-α and IL-1β and phosphorylation of p38, JNK, ERK and p65 (or nuclear translocation of p65). We demonstrated that nucleolin mediated the LPS-induced activation of MAPK and NF-κB signaling pathways, and regulated the secretion of inflammatory mediators (TNF-α, IL-1β and HMGB1).

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“…SAL has been confirmed osseointegration and anti-inflammatory activities used in the treatment of a variety of diseases, such as bone defect, fracture, arthritis, etc. [ 14 ]. The mechanism may be related to the inhibition of NF-κB phosphorylation by SAL, which affects a series of related signaling pathways.…”

Section: Introductionmentioning

confidence: 99%

Improvement of polydopamine-loaded salidroside on osseointegration of titanium implants

Liang

Dong

et al. 2022

Chin Med

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Background Microarc oxidation (MAO) on the surface of medical pure titanium can improve its histocompatibility, and loading drugs on the surface can resist excessive intimal hyperplasia. Methods In this study, salidroside (SAL) was loaded on the surface of porous titanium (Ti) with polydopamine (PDA) carrier. The effects of SAL on the osteogenesis and angiogenesis of Ti implants were studied by phalloidin staining, alizarin red staining, ALP staining, wound-healing assay, cell transwell assay, matrigel tube formation, and osteogenic and angiogenic genes and proteins expression detected by PCR and western blot in vitro. The bone defect model experiments in rats was established in vivo including X-ray, micro CT, hematoxylin and eosin staining (HE), immunohistochemistry (IHC), Goldner's trichrome analysis, Safranin O-fast green staining and determination of contents of TNF-α and IL-6 in serum. Results EDS and EDS mapping showed that SAL could be loaded on the surface of the MAO coating by PDA. A drug release experiment showed that SAL loaded on the Ti coating could release slowly and stably without sudden release risk. In vitro cell experiments showed that the SAL coating could promote the proliferation, morphology, calcification and alkaline phosphate activity of MC3T3-E1 cells. At the same time, it promoted the migration and tube formation of HUVEC cells. The SAL coating promoted osteogenesis and angiogenesis by promoting the expression of genes and proteins related to. In vivo experiments, HE and IHC showed that SAL significantly promoted the expression of COL-1 and CD31. Goldner's trichrome and Safranin O-fast green staining showed that SAL coating could increase the new bone tissue around the implantation site. The SAL coating had anti-inflammatory activity by reducing the levels of TNF-α and IL-6 in vivo. Conclusion Therefore, SAL could improve osteogenesis and angiogenesis in conjunction with the Ti-PDA coating.

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Salidroside Inhibits Lipopolysaccharide-ethanol-induced Activation of Proinflammatory Macrophages via Notch Signaling Pathway

Cited by 22 publications

References 38 publications

Mechanism and Experimental Verification of the Use of Rhodiola crenulata to Cytokine Storm Based on Network Pharmacology and Molecular Docking

Mechanism and Experimental Verification of the Use of Rhodiola crenulata to Cytokine Storm Based on Network Pharmacology and Molecular Docking

Nucleolin Mediates LPS-induced Expression of Inflammatory Mediators and Activation of Signaling Pathways

Improvement of polydopamine-loaded salidroside on osseointegration of titanium implants

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