Monoammonium glycyrrhizate suppresses tumor necrosis factor-α induced chemokine production in HMEC-1 cells, possibly by blocking the translocation of nuclear factor-κB into the nucleus

Cao, Na; Chen, Tao; Guo, Zhanfang; Qin, Si; Li, Mengmeng

doi:10.1139/cjpp-2014-0022

Cited by 7 publications

(6 citation statements)

References 19 publications

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“…Cimato et al (24) found that inflammatory cytokines, rather than cholesterol, regulated the expression of CX3CL1 in atherosclerosis. Cao et al suggested that human dermal microvascular endothelial cell-1 in patients with inflammatory skin disease induced chemokines, including CXCL8, CX3CL1 and CXCL16, by activating the NF-κB signaling pathway when stimulated by TNF-α, which is in agreement with our previous finding that LPS-NF-κB-CX3CL1 exists in human bronchial epithelial cells (5,25). The present study revealed that CX3CL1-shRNA inhibited the secretion of NF-κB in the thrombus-stimulated LMVEC model, which was also consistent with a previous report (26).…”

Section: Discussionsupporting

confidence: 92%

Aspirin modulates the inflammatory response in a thrombus‑stimulated LMVEC model

Wang

Ying²,

Jiang

et al. 2018

Int J Mol Med

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The purpose of the present study was to examine whether aspirin interferes with the inflammatory response in a thrombus-stimulated lung microvascular endothelial cell (LMVEC) model. The LMVECs were randomly divided into eight groups: Normal group (group N), model group (group M), model + ASP group (group M+A), model+CX3CL1-short hairpin (sh)RNA group (group M+SH), model + CX3CL1-overexpression vector group (group M+CX3), model + ASP + shRNA group (group M+A+SH), model + ASP + CX3CL1-overexpression vector group (group M+A+CX3), and normal + virus control group (group N+V). The endothelial cells were cultured, and a thrombus was added to the cells. Briefly, 12 h following the precipitation of the thrombus, data from ELISA, reverse transcription-quantitative polymerase chain reaction analysis and confocal microscopy revealed that the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, CX3C chemokine ligand 1 (CX3CL1), CX3C chemokine receptor 1 (CX3CR1) and nuclear factor-κB (NF-κB) in group M were increased, compared with those in group N (P<0.01). These levels, with the exception of TNF-α, were significantly lower in group M+SH, compared with those in group M (P<0.01). Furthermore, the levels of IL-6 in groups M+A, M+CX3 and M+A+CX3 were decreased, compared with those in group M (P<0.01); the level of TNF-α in group M+A+SH was decreased, compared with that in group M (P<0.01); the level of CX3CR1 waslower in groups M+A and M+A+SH, compared with that in group M (P<0.01), and the level of NF-κB in group M+SH was decreased, compared with the level in group M and group M+A (P<0.05). In conclusion, the thrombus-stimulated LMVEC model exhibited induced production of TNF-α, IL-6, CX3CL, CX3CR1, NF-κB and intercellular adhesion molecule-1. Furthermore, it was confirmed that the signaling pathways involving CX3CL1-NF-κB, IL-6 and TNF-α were partly inhibited by aspirin.

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Section: Discussionsupporting

confidence: 92%

Aspirin modulates the inflammatory response in a thrombus‑stimulated LMVEC model

Wang

Ying²,

Jiang

et al. 2018

Int J Mol Med

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“…Glycyrrhizin has been confirmed to have both anti-inflammatory and anti-viral influences by combining directly to HMGB1, and inhibits its chemoattractant and mitogenic activities ( 15 ). Our previous study found that glycyrrhizin suppresses TNF- α induced chemokine production in HMEC-1 cells ( 16 ). We also found that the serum HMGB1 level of 16 Henoch– Schonlein purpura patients was significantly lower after treatment with glycyrrhizin ( 11 ).…”

Section: Introductionmentioning

confidence: 99%

The Anti-inflammatory Effects of HMGB1 Blockades in a Mouse Model of Cutaneous Vasculitis

Wang

Yang

et al. 2020

Front. Immunol.

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In our previous study, we have found increased serum levels of HMGB1 in patients with Henoch– Schonlein purpura (HSP), allergic vasculitis (AV), and urticarial vasculitis (UV) and altered HMGB1 distribution in lesional skin in patients with HSP. HMGB1 plays a pro-inflammatory role in the pathogenesis of HSP. To further investigate the role of HMGB1 in the pathogenic mechanism of vasculitis, we investigated the anti-inflammatory effects of HMGB1 blockades (including anti-HMGB1 mAb and glycyrrhizin) in a mouse model of a cutaneous reverse passive Arthus (RPA) reaction. A total of 36 balb/c mice were randomly divided into four groups: the control group, IC model group, HMGB1 monoclonal antibody (anti-HMGB1-mAb) group and the glycyrrhizin group, with nine mice in each group. A cutaneous RPA reaction mouse model was established by injections of the OVA antibody and the OVA antigen. Mice of the anti-HMGB1-mAb group and glycyrrhizin group were pre-treated with anti-HMGB1 mAb or glycyrrhizin, respectively, before the RPA reaction. Our results indicated that HMGB1 blockades (anti-HMGB1 mAb and glycyrrhizin) obviously extenuated the severity of vasculitis skin damage and improved the histological evolvement of inflammatory cells infiltration, vascular fibroid necrosis, and vasodilation in a cutaneous RPA reaction mouse model. In addition, HMGB1 blockades reduced the infiltration of neutrophils, DCs, and T cells and decreased the mRNA expression of IL-6 and CCL5 in skin lesions in the cutaneous RPA reaction mouse model. We suggest that HMGB1 blockades may represent a new direction for the treatment of cutaneous vasculitis.

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“…Recent studies have indicated that DPMCs and macrophages can stimulate angiogenesis through potent pro-angiogenic factors, and secretory DPMCs, macrophages and T cells have also been noted to affect adjacent non-endothelial cells or to recruit each other via chemotactic signals, and these potential factors jointly maintain the stability of the skin microenvironment ( 34 , 35 ).Marvelous ultrastructural changes appeared during xenobiotics attack. Pericytes underwent tighter junctions with DMECs but did not generate the pathological changes of gap formation ( 9 , 10 , 36 – 40 ). We tend to identify it as a physiological change caused by altered local permeability pressure after needle-free injection, since pericytes play an important role in regulating microvascular permeability, which would permit more hemolymph exchange to proceed ( 41 ).…”

Section: Discussionmentioning

confidence: 96%

“…Ultrastructural evidences suggest that the center of DMUs is composed of DMECs that originate from the horizontal papillary plexuses ( 6 ). These structures are responsible for the blood supply to the dermis stratum papillare and are responsive to injury ( 7 ), hypoxia ( 8 ), and stress ( 9 , 10 ), which manifests in the ultrastructure by gap formation and altered deposition in the basement membrane material of the vascular wall ( 11 – 13 ). Pericytes are located adjacent to or above endothelial cell junctions, which can control the contraction of DMECs by upregulating endothelin-1 (ET-1) and downregulating of iNOS expressed by DMECs ( 14 , 15 ).…”

Section: Introductionmentioning

confidence: 99%

Dermal Microvascular Units in Domestic Pigs (Sus scrofa domestica): Role as Transdermal Passive Immune Channels

et al. 2022

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The dermal microvascular unit (DMU) is a perivascular functional unit in the dermis. It is composed of microvascular and capillary lymphatics surrounded by immune cells. In this study, jet needle-free injection system was used to injected biocompatible carbon nanoparticles into the cervical skin of domestic pigs (Sus scrofa domestica) and assessed the morphological distribution of DMUs by hematoxylin erythrosine staining, immunohistochemistry (IHC), and transmission electron microscopy (TEM), and TEM was also used to observe the ultrastructural changes of DMUs after jet needle-free injection. Following our study, we identified DMUs in the dermis stratum papillare and similar structures in the dermis stratum reticulare, but the aggregation of CD68+ and CD1a+ cells in the dermis stratum papillare of DMUs by IHC confirmed that DMUs act as reservoirs of dermal immune cells, while similar structures in the dermis stratum reticulare should not be considered as DMUs. Ultrastructure of DMUs was revealed by TEM. Marvelous changes were found following xenobiotics attack, including the rearrangement of endothelial cells and pericytes, and the reactivity of immune cells. Novel interstitial cell telocyte (TC) was also identified around the microvasculature, which may have been previously known as the veil cell. Our results successfully identified the distribution of DMUs in the skin of domestic pigs, which might act as reservoirs of immune cells in the skin and play a role in immune surveillance and immune defense.

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Monoammonium glycyrrhizate suppresses tumor necrosis factor-α induced chemokine production in HMEC-1 cells, possibly by blocking the translocation of nuclear factor-κB into the nucleus

Cited by 7 publications

References 19 publications

Aspirin modulates the inflammatory response in a thrombus‑stimulated LMVEC model

Aspirin modulates the inflammatory response in a thrombus‑stimulated LMVEC model

The Anti-inflammatory Effects of HMGB1 Blockades in a Mouse Model of Cutaneous Vasculitis

Dermal Microvascular Units in Domestic Pigs (Sus scrofa domestica): Role as Transdermal Passive Immune Channels

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