veronicastroside and Inflammation

The present study aimed to evaluate anti-rheumatoid arthritis (RA) effect of Lonicerin (LON), a safe compound with anti-inflammatory and immunomodulatory properties. Nevertheless, the exact role of LON in RA remains elusive. In this test, the anti-RA effect of LON was evaluated in collagen-induced arthritis (CIA) mouse model. Relevant parameters were measured during the experiment; ankle tissue and serum were collected at the end of the experiment for radiology, histopathology, and inflammation analysis. ELISA, qRT-PCR, immunofluorescence, and western blot were used to explore the effect of LON on the polarization of macrophages and related signal pathways. It was discovered that LON treatment attenuated the disease progression of CIA mice with lower paw swelling, clinical score, mobility, and inflammatory response. LON treatment significantly decreased M1 marker levels in CIA mice and LPS/IFN-γ-induced RAW264.7 cells, while slightly increasing M2 marker levels in CIA mice and IL-4-induced RAW264.7 cells. Mechanistically, LON attenuated the activation of the NF-κB signaling pathway, which contributes to M1 macrophage polarization and inflammasome activation. In addition, LON inhibited NLRP3 inflammasome activation in M1 macrophages, thereby reducing inflammation by inhibiting IL-1β and IL-18 release. These results indicated that LON might exert anti-RA effects by regulating the polarization of M1/M2 macrophage, especially by inhibiting macrophage polarization toward M1.

Topics: Animals; Arthritis, Experimental; Arthritis, Rheumatoid; Inflammasomes; Inflammation; Macrophages; Mice; NF-kappa B; Signal Transduction

Acute lung injury (ALI) is a life-threatening condition caused by severe inflammation of lung tissues. We hypothesized that lipopolysaccharide induced acute lung inflammation and injury in mice might be controlled by lonicerin (LCR), a plant flavonoid that impacts immunity, oxidative stress, and cell proliferation. LCR reduced pathological changes including pulmonary edema, elevation of protein in bronchoalveolar lavage, inflammation, pro-inflammatory gene expression, expression of toll-like receptor 4/nuclear factor-kappa B, apoptosis, and significantly reduced mortality. Together, the results suggest that LCR might be a potential and effective candidate for the treatment of ALI that acts by inhibiting inflammation and apoptosis.

Topics: Acute Lung Injury; Animals; Apoptosis; Cytokines; Gene Expression; Humans; Inflammation; Lipopolysaccharides; Lung; Luteolin; Male; Mice, Inbred C57BL; NF-kappa B; Survival Rate; Toll-Like Receptor 4

The aim of this study was to investigate the effects of two structurally related flavonoids found in Cyclopia subternata, vicenin-2 (VCN) and scolymoside (SCL) on lipopolysaccharide (LPS)-induced liver failure in mice and to elucidate underlying mechanisms. Mice were treated intravenously with VCN or SCL at 12 h after LPS treatment. LPS significantly increased mortality, serum levels of alanine transaminase, aspartate transaminase, and inflammatory cytokines, and toll-like receptor 4 (TLR4) protein expression; these effects of LPS were inhibited by VCN or SCL. It also attenuated the LPS-induced activation of myeloid differentiation primary response gene 88 and TLR-associated activator of interferon-dependent signaling pathways of the TLR system. Our results suggest that VCN or SCL protects against LPS-induced liver damage by inhibiting the TLR-mediated inflammatory pathway, indicating its potential to treat liver diseases.

Topics: Animals; Apigenin; Glucosides; Inflammation; Lipopolysaccharides; Luteolin; Male; Mice; Signal Transduction

The vascular inflammatory process has been suggested to play a key role in the initiation and progression of atherosclerosis, a major complication of diabetes mellitus. Thus, in this study, we attempted to determine whether 2 structurally related flavonoids found in Cyclopia subternata, vicenin-2 and scolymoside, can suppress high-glucose (HG)-induced vascular inflammatory processes in human umbilical vein endothelial cells (HUVECs) and mice. The effects of vicenin-2 and scolymoside on HG-induced vascular inflammation were determined by measuring vascular permeability, leukocyte adhesion and migration, cell adhesion molecule (CAM) expression levels, and reactive oxygen species (ROS) formation. In addition, the anti-inflammation mechanism was investigated using immunofluorescence staining and Western blotting. The data showed that HG markedly increased vascular permeability, monocyte adhesion, expression of CAMs, formation of reactive oxygen species (ROS), and activation of nuclear factor (NF)-κB. Remarkably, pretreatment with vicenin-2 and scolymoside attenuated all of the above-mentioned vascular inflammatory effects of HG. HG-induced vascular inflammatory responses are critical events underlying the development of various diabetic complications; therefore, our results suggest that vicenin-2 and scolymoside have significant therapeutic benefits against diabetic complications and atherosclerosis.

Topics: Animals; Anti-Inflammatory Agents; Apigenin; Capillary Permeability; Cell Adhesion; Cell Adhesion Molecules; Cells, Cultured; Flavonoids; Glucose; Glucosides; Human Umbilical Vein Endothelial Cells; Humans; Inflammation; Inflammation Mediators; Luteolin; Male; Mice; Mice, Inbred C57BL; Monocytes; NF-kappa B; Reactive Oxygen Species