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Atherosclerosis is a major cause of coronary heart disease. As a result of the development of atherosclerotic lesions, the walls of blood vessels become thicker and inhibit blood circulation. Atherosclerosis is caused by a high-fat diet and vascular injury. Chronic arterial inflammation plays an important role in the pathogenesis of atherosclerosis. In particular, secretion of the pro-atherogenic cytokine tumor necrosis factor-α induces expression of endothelial adhesion molecules including P-selectin, vascular cell adhesion molecule 1 (VCAM-1), and intercellular adhesion molecule 1 (ICAM-1), which mediate attachment of circulating monocytes and lymphocytes. In this study, we examined the anti-atherosclerotic effect of sorghum, which is known to have anti-oxidant and anti-inflammatory activity. A 50% ethanol extract of Sorghum bicolor L. Moench fermented with Aspergillus oryzae NK (fSBE) was used for experiments. In vitro expression of endothelial adhesion molecules VCAM-1 and ICAM-1 and pro-inflammatory factor cyclooxygenase-2 was significantly decreased and that of the anti-atherogenic factor heme oxygenase-1 significantly increased by fSBE (P < 0.05). At the in vivo level, we examined fat droplets of liver tissue, and aortic thickness via histological analysis, and determined the blood lipid profile through chemical analysis. fSBE at a dose of 200 mg/kg significantly improved blood and vascular health (P < 0.05). Taken together, these results demonstrate that fSBE has potential as a therapeutic anti-atherosclerotic agent. [ABSTRACT FROM AUTHOR]

Tumor necrosis factor-α (TNF-α) plays an important role in inflammatory responses. Deregulated activation of TNF-α signaling is associated with various inflammatory diseases. In view of the finding that the seventy percent ethanol extract of Litsea japonica (LJE) interferes with TNF-α-induced NF-κB activation, activity- guided fractionation was performed to identify the active components of the extract. The EtOAc, CHCl and n-Hexane fractions of LJE induced suppression of inhibitor of κB (IκB) kinase (IKK), p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK), and significant reduction of TNF-α- induced NF-κB activation. From the CHCl fraction, hamabiwalactone A, hamabiwalactone B, litsenolide B2 and litsenolide C2 were identified to inhibit TNF- α-induced NF-κB activation. The cytotoxic activities of these lactone compounds were additionally evaluated. [ABSTRACT FROM AUTHOR]

Surfactin is primarily produced by Bacillus natto TK-1 and is one of the most powerful biosurfactants. It consists of a heptapeptide interlinked with a β-hydroxy fatty acid. Because of its special structure, surfactin shows broad biological effects, including anti-tumour, anti-microbial and anti-mycoplasma activities. It also has potential anti-inflammatory activity; however, the anti-inflammatory mechanism of surfactin has not been explored. In this study, we investigated the anti-inflammatory mechanism of surfactin in lipopolysaccharide (LPS)-stimulated macrophages. Surfactin exhibited an anti-inflammatory effect without cytotoxicity at certain concentrations, and the lipopolysaccharide (LPS)-stimulated cells appeared normal after surfactin treatment. Surfactin significantly inhibited the increased expression of IFN-γ, IL-6, iNOS and nitric oxide (NO). TLR4 is the critical receptor for LPS; therefore, the TLR4 signal transduction pathway is the primary pathway that mediates LPS-induced inflammation. The results show that surfactin downregulated the LPS-induced TLR4 protein expression of macrophages and indicated that the surfactin-mediated signal pathway was involved in with TLR4. The subsequent studies demonstrated that surfactin exhibited anti-inflammatory effects by attenuating the activation of nuclear factor-κB (NF-κB), which is involved in the nuclear factor-κB (NF-κB) cell signalling pathways. These results suggest that surfactin may be a new therapeutic agent for inflammation. [ABSTRACT FROM AUTHOR]

Osteoporosis is recognized as a major concern among menopausal women and the elderly. When estrogen is reduced in the body, local factors such as IL-1(β, IL-6 and PGE2, which are known to be related to bone resorption, are increased and promote osteoclastogenesis, which is responsible for bone resorption and results in the clinical disorder osteoporosis. In this study, we investigated the anti-osteoporotic activity of Ficus erecta. MG-63 cells were stimulated with IL-iβ (10 ng/mL) to induce osteoporotic factors (IL-6, COX-2 and PGE2) and RAW 264.7 cells were stimulated with RANKL (100 ng/mL) to induce their differentiation into osteoclasts. We found F. erecta fractions decreased the mRNA expression of IL-6 and COX-2, and protein levels of COX-2 and PGE2 production. Among sequential solvent fractions, hexane and EtOAc fractions decreased differentiation into osteoclasts of RAW 264.7 cells. These results suggest that F. erecta may have significant effects on osteoporotic factors and may be provided as a possible anti-osteoporotic therapeutic plant. [ABSTRACT FROM AUTHOR]

The anti-inflammatory activity of Eurya emarginata (Thumb) Makino, of which leaves have been traditionally used to treat ulcers or diuretic in Jeju Island, has been investigated in the present study. Through the phytochemical study from the methanol extract of E emaginiata, eutigosides and were isolated as the active components. Sseveral inflammatory markers including TNF-α, IL 1β, IL-6, NO, INOS, and COX-2 were examined. Eutigosides and potentially inhibited production of pro-inflammatory cytokines (IL-6 and TNF-α) in a dose-dependent manner. Additionally, the intracellular contents of INOS protein were markedly decreased after treatment with eutigosides and The inhibition of iNOS activity was correlated with the decrease in nitrite levels. These results suggest that eutigoside and from E. emarginata may have anti-inflammatory activity through the inhibition of pro-inflammatory cytokines (TNF-α and IL-6), INOS and COX-2. [ABSTRACT FROM AUTHOR]