Geniposide inhibits interleukin-6 and interleukin-8 production in lipopolysaccharide-induced human umbilical vein endothelial cells by blocking p38 and ERK1/2 signaling pathways

Liu, Hongtao; He, Junlin; Li, Wenming; Yang, Zhu; Wang, Yingxiong; Yin, Juan Juan; Du, Yifeng

doi:10.1007/s00011-009-0118-3

Cited by 48 publications

(33 citation statements)

References 36 publications

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“…Our results suggest that the inhibitory effect of geniposide on cell adhesion may be related to inhibition of the NF-κB signal pathway. More recently, Liu et al reported that geniposide inhibits interleukin-6 and interleukin-8 production in lipopolysaccharide-induced HUVECs by blocking p38 and ERK1/2 signaling pathways [34] . In addition to ROS and the NF-κB pathway, extracellular regulated protein kinase (ERK), C-jun N-terminal kinase (JNK) and p38, the main members of mitogen-activated protein kinase (MAPK) family, may also be involved in high glucose-induced VCAM-1 and E-selectin expression.…”

Section: Discussionmentioning

confidence: 99%

Geniposide inhibits high glucose-induced cell adhesion through the NF-κB signaling pathway in human umbilical vein endothelial cells

Wang

Xü

et al. 2010

Acta Pharmacol Sin

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Aim: To investigate whether geniposide, an iridoid glucoside extracted from gardenia jasminoides ellis fruits, inhibits cell adhesion to human umbilical vein endothelial cells (HUVECs) induced by high glucose and its underlying mechanisms. Methods: HUVECs were isolated from human umbilical cords and cultured. The adhesion of monocytes to HUVECs was determined using fluorescence-labeled monocytes. The mRNA and protein levels of vascular cell adhesion molecule-1 (VCAM-1) and endothelial selectin (E-selectin) were measured using real-time RT-PCR and ELISA. Reactive oxygen species (ROS) production was measured using a fluorescent probe. The amounts of nuclear factor-kappa B (NF-κB) and inhibitory factor of NF-κB (IκB) were determined using Western blot analysis. The translocation of NF-κB from the cytoplasm to the nucleus was determined using immunofluorescence. Results: Geniposide (10-20 µmol/L) inhibited high glucose (33 mmol/L)-induced adhesion of monocytes to HUVECs in a dose-dependent manner. This compound (5-40 µmol/L) also inhibited high glucose-induced expression of VCAM-1 and E-selectin at the gene and protein levels. Furthermore, geniposide (5-20 µmol/L) decreased ROS production and prevented IκB degradation in the cytoplasm and NF-κB translocation from the cytoplasm to the nucleus in HUVECs. Conclusion: Geniposide inhibits the adhesion of monocytes to HUVECs and the expression of CAMs induced by high glucose, suggesting that the compound may represent a new treatment for diabetic vascular injury. The mechanism underlying this inhibitory effect may be related to the inhibition of ROS overproduction and NF-κB signaling pathway activation by geniposide.

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Section: Discussionmentioning

confidence: 99%

Geniposide inhibits high glucose-induced cell adhesion through the NF-κB signaling pathway in human umbilical vein endothelial cells

Wang

Xü

et al. 2010

Acta Pharmacol Sin

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“…Geniposide, an iridoid glucoside, is a major component ( ≥ 2%) in the fruits of G. jasminoides Ellis. Until now, pharmacological studies of geniposide have revealed key properties, including antitumor effects (Hsu et al, 1997), modulation of DNA expression (Galvez et al, 2005), treatment of pain (Gong et al, 2014), and anti-inflammatory, coloretic, and hepatoprotective effects (Chou et al, 2003;Chen et al, 2009;Liu et al, 2010;Ma et al, 2011). However, the precise mechanisms of its effects remain poorly understood.…”

Section: Metabolism and Pharmacokineticsmentioning

confidence: 99%

Neuroprotective effects of geniposide on Alzheimer’s disease pathology

Liu

Hölscher³

et al. 2015

Reviews in the Neurosciences

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AbstractA growing body of evidence has linked two of the most common aged-related diseases: type 2 diabetes mellitus (T2DM) and Alzheimer’s disease (AD). It has led to the notion that drugs developed for the treatment of T2DM may be beneficial in modifying the pathophysiology of AD. As a receptor agonist of glucagon-like peptide-1 (GLP-1R), which is a newer drug class to treat T2DM, geniposide shows clear effects in inhibiting pathological processes underlying AD, such as promoting neurite outgrowth. In the present article, we review the possible molecular mechanisms of geniposide to protect the brain from pathologic damages underlying AD: reducing amyloid plaques, inhibiting τ phosphorylation, preventing memory impairment and loss of synapses, reducing oxidative stress and the chronic inflammatory response, and promoting neurite outgrowth via the GLP-1R signaling pathway. In summary, the Chinese herb geniposide shows great promise as a novel treatment for AD.

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“…Notably, HUVECs are involved in the release of cytokines and chemokines, as well as cell migration during the inflammatory process (4,5). Increased levels of vascular cell adhesion molecule-1 (VCAM-1) and intracellular adhesion molecule-1 (ICAM-1) are early markers of endothelial activation and dysfunction in inflammatory diseases (6).…”

Section: Introductionmentioning

confidence: 99%

Effect of arazyme on the lipopolysaccharide-induced inflammatory response in human endothelial cells

Kim

Yang

Shin

et al. 2014

Molecular Medicine Reports

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Abstract. Arazyme is a novel extracellular metalloprotease secreted by Aranicola proteolyticus. Endothelial cells are involved in the pathogenesis of a number of inflammatory diseases, induce uncontrolled cell viability and express various inflammatory mediators, including cytokines, chemokines, adhesion molecules and reactive oxygen species (ROS). In the current study, human umbilical vein endothelilal cells (HUVECs) were used to investigate the anti-inflammatory effects of arazyme following lipopolysaccharide (LPS) stimulation. Apoptosis of HUVECs due to LPS was inhibited by arazyme. In various inflammatory responses induced by LPS, arazyme inhibited the secretion of the monocyte chemoattractant protein-1 and interleukin-6, and the expression of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1. Arazyme also suppressed ROS production in HUVECs. The action of arazyme was not associated with NF-κB activity in HUVECs. These results indicate that arazyme has anti-inflammatory properties in inflamed endothelial cells and may be useful as a therapeutic agent for inflammatory diseases associated with endothelial cells.

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Geniposide inhibits interleukin-6 and interleukin-8 production in lipopolysaccharide-induced human umbilical vein endothelial cells by blocking p38 and ERK1/2 signaling pathways

Abstract: The results show that geniposide can inhibit LPS-induced IL-6 and IL-8 production in HUVECs by blocking p38 MAPK and ERK1/2 signaling pathways.

Cited by 48 publications

References 36 publications

Geniposide inhibits high glucose-induced cell adhesion through the NF-κB signaling pathway in human umbilical vein endothelial cells

Geniposide inhibits high glucose-induced cell adhesion through the NF-κB signaling pathway in human umbilical vein endothelial cells

Neuroprotective effects of geniposide on Alzheimer’s disease pathology

Effect of arazyme on the lipopolysaccharide-induced inflammatory response in human endothelial cells

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