• IMMUNE NETWORK
• /
• v.9 no.3
• /
• pp.98-105
• /
• 2009

Background: It has been recently noticed that type 2 diabetes (T2D), one of the most common metabolic diseases, causes a chronic low-grade inflammation and activation of the innate immune system that are closely involved in the pathogenesis of T2D. Cordyceps militaris, a traditional medicinal mushroom, produces a component compound, cordycepin (3'-deoxyadenosine). Cordycepin has been known to have many pharmacological activities including immunological stimulating, anti-cancer, and anti-infection activities. The molecular mechanisms of cordycepin in T2D are not clear. In the present study, we tested the role of cordycepin on the anti-diabetic effect and anti-inflammatory cascades in LPS-stimulated RAW 264.7 cells. Methods: We confirmed the levels of diabetes regulating genes mRNA and protein of cytokines through RT-PCR and western blot analysis and followed by FACS analysis for the surface molecules. Results: Cordycepin inhibited the production of NO and pro-inflammatory cytokines such as IL-$1{\beta}$, IL-6, and TNF-${\alpha}$ in LPS-activated macrophages via suppressing protein expression of pro-inflammatory mediators. T2D regulating genes such as $11{\beta}$-HSD1 and PPAR${\gamma}$ were decreased as well as expression of co-stimulatory molecules such as ICAM-1 and B7-1/-2 were also decreased with the increment of its concentration. In accordance with suppressed pro-inflammatory cytokine production lead to inhibition of diabetic regulating genes in activated macrophages. Cordycepin suppressed NF-${\kappa}B$ activation in LPS-activated macrophages. Conclusion: Based on these observations, cordycepin suppressed T2D regulating genes through the inactivation of NF-${\kappa}B$ dependent inflammatory responses and suggesting that cordycepin will provide potential use as an immunomodulatory agent for treating immunological diseases.

• Biomolecules & Therapeutics
• /
• v.22 no.6
• /
• pp.547-552
• /
• 2014

Ribes fasciculatum var. chinense MAX. (R. fasciculatum) has traditionally been used in Korea to treat inflammatory diseases. However, the exact mechanism that accounts for the anti-inflammatory effect of R. fasciculatum is not completely understood. We aimed to ascertain the pharmacological effects of R. fasciculatum on both compound 48/80- or histamine-induced scratching behaviors and 2, 4-dinitrochlorobenzene (DNCB)-induced atopic dermatitis (AD) in mice. Additionally, to find a possible explanation for the anti-inflammatory effects of R. fasciculatum, we evaluated the effects of R. fasciculatum on the production of inflammatory mediators in LPS-stimulated macrophage cells. Treatment of R. fasciculatum significantly reduced compound 48/80- or histamine-induced the pruritus in mice. R. fasciculatum attenuated the AD symptoms such as eczematous, erythema and dryness and serum IgE levels in AD model. Additionally, R. fasciculatum inhibited the production of tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) and interleukin-6 (IL-6). The maximal rates of TNF-${\alpha}$ and IL-6 inhibition by R. fasciculatum (1 mg/ml) were approximately 32.12% and 46.24%, respectively. We also showed that R. fasciculatum inhibited the activation of nuclear factor-kappa B in LPS-stimulated macrophages. Collectively, the findings of this study provide us with novel insights into the pharmacological actions of R. fasciculatum as a potential molecule for use in the treatment of allergic inflammatory diseases.

• Proceedings of the Plant Resources Society of Korea Conference
• /
• 2019.10a
• /
• pp.67-67
• /
• 2019

Vaccinium oldhamii (V. oldhamii) has been reported to exert a variety of the pharmacological properties such as anti-oxidant activity, anti-cancer activity, and inhibitory activity of ${\alpha}$-amylase and acetylcholinesterase. However, the anti-inflammatory activity of V. oldhamii has not been studied. In this study, we aimed to investigate anti-inflammatory activity of the stem extracts from V. oldhamii, and to elucidate the potential mechanisms in LPS-stimulated RAW264.7 cells. Among VOS, VOL and VOF, the inhibitory effect of NO and PGE2 production induced by LPS was highest in VOS treatment. Thus, VOS was selected for the further study. VOS dose-dependently blocked LPS-induced NO and PGE2 production by inhibiting iNOS and COX-2 expression, respectively. VOS inhibited the expression of pro-inflammatory cytokines such as $IL-1{\beta}$, IL-6 and $TNF-{\alpha}$. In addition, VOS suppressed TRAP activity and attenuated the expression of the osteoclast-specific genes such as NFATc1, c-FOS, TRAP, MMP-9, cathepsin K, CA2, OSCAR and ATPv06d2. VOS inhibited LPS-induced $NF-{\kappa}B$ signaling activation through blocking $I{\kappa}B-{\alpha}$ degradation and p65 nuclear accumulation. VOS inhibited MAPK signaling activation by attenuating the phosphorylation of ERK1/2, p38 and JNK. Furthermore, VOS inhibited ATF2 phosphorylation and blocked ATF2 nuclear accumulation. From these findings, VOS has potential to be a candidate for the development of chemopreventive or therapeutic agents for the inflammatory diseases.

• Journal of Microbiology and Biotechnology
• /
• v.32 no.1
• /
• pp.81-90
• /
• 2022

Peucedanum japonicum Thunberg (PJT) has been used in traditional medicine to treat colds, coughs, fevers, and other inflammatory diseases. The goal of this study was to investigate whether 3'-isovaleryl-4'-senecioylkhellactone (IVSK) from PJT has anti-inflammatory effects on lung epithelial cells. The anti-inflammatory effects of IVSK were evaluated using phorbol 12-myristate 13-acetate (PMA)-stimulated A549 cells and regular human lung epithelial cells as a reference. IVSK reduced the secretion of the inflammatory mediators interleukin (IL)-8 and monocyte chemoattractant protein-1 (MCP-1), and the mRNA expression of IL-6, IL-8, MCP-1, and IL-1β. Additionally, it inhibited the phosphorylation of IκB kinase (IKK), p65, Iκ-Bα, and mitogen-activated protein kinases (MAPKs) p38, JNK, and ERK in A549 cells stimulated with PMA. Moreover, the binding affinity of activator protein-1 (AP-1) and nuclear factor-κB (NF-κB) was significantly reduced in the luciferase assay, while nuclear translocation was markedly inhibited by IVSK in the immunocytochemistry. These findings indicate that IVSK can protect against inflammation through the AP-1 and NF-κB pathway and could possibly be used as a lead compound for the treatment of inflammatory lung diseases.

• Journal of Ginseng Research
• /
• v.46 no.5
• /
• pp.690-699
• /
• 2022

Background: Few studies reported the therapeutic effect of Korean Red Ginseng (KRG) in lung inflammatory diseases. However, the anti-inflammatory role and underlying molecular in cadmium-induced lung injury have been poorly understood, directly linked to chronic lung diseases (CLDs): chronic obstructive pulmonary disease (COPD), cancer etc. Therefore, in this study we aim to investigate the therapeutic activities of water extract of KRG (KRG-WE) in mouse cadmium-induced lung injury model. Method: The anti-inflammatory roles and underlying mechanisms of KRG-WE were evaluated in vitro under cadmium-stimulated lung epithelial cells (A549) and HEK293T cell line and in vivo in cadmium-induced lung injury mouse model using semi-quantitative polymerase chain reaction (RT-PCR), quantitative real-time PCR (qPCR), luciferase assay, immunoblotting, and FACS. Results: KRG-WE strongly ameliorated the symptoms of CdSO4-induced lung injury in mice according to total cell number in bronchoalveolar lavage fluid (BALF) and severity scores as well as cytokine levels. KRG-WE significantly suppressed the upregulation of inflammatory signaling comprising mitogen-activated protein kinases (MAPK) and their upstream enzymes. In in vitro study, KRG-WE suppressed expression of interleukin (IL)-6, matrix metalloproteinase (MMP)-2, and IL-8 while promoting recovery in CdSO₄-treated A549 cells. Similarly, KRG-WE reduced phosphorylation of MAPK and c-Jun/c-Fos in cadmium-exposed A549 cells. Conclusion: KRG-WE was found to attenuate symptoms of cadmium-induced lung injury and reduce the expression of inflammatory genes by suppression of MAPK/AP-1-mediated pathway.

• The Korea Journal of Herbology
• /
• v.33 no.4
• /
• pp.35-41
• /
• 2018

Objectives : Hyeonggaeyeongyotang Gagambang (HYT) is a herbal medicine prescribed for the treatment of inflammatory diseases, but it is necessary to study the exact therapeutic efficacy. This study aims to investigate the antibacterial and anti-inflmmatory activities of HYT. Methods : Antibacterial activity of HYT was confirmed by staining Escherichia coli, a gram negative strain, and Staphylococcus aureus, a gram positive strain, on solid Lysogeny Broth (LB) medium containing HYT. Antioxidant activity of HYT was confirmed by 2,2'-azino-bis-3-ethylbenzothiazoline-6-sulphonic acid (ABTS) assay. The phosphorylation of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha ($I{\kappa}B{\alpha}$) after lipopolysaccharide (LPS) treatment with HYT-treated RAW 264.7 mouse macrophages cells was confirmed by immunoblot analysis and the level of interleukin 1 beta (IL-$1{\beta}$) mRNA expression level was confirmed by quantitative real-time PCR. Results : HYT showed a concentration-dependent antibacterial activity against Escherichia coli and Staphylococcus aureus and also showed excellent antioxidant activity. HYT treatment attenuated the phosphorylation of $I{\kappa}B{\alpha}$induced by LPS treatment in RAW 264.7 mouse macrophages cells. The phosphorylation of $I{\kappa}B{\alpha}$is crucial for the regulation of the expression of various pro-inflammatory cytokines. In addition, IL-$1{\beta}$ mRNA expression level of RAW 264.7 mouse macrophages cells stimulated by LPS treatment was also inhibited by HYT treatment. Conclusions : Through experimental demonstration of the antioxidative, antimicrobial and anti-inflammatory effects of HYT, we demonstrated that HYT is a herbal medicine effective for the treatment of inflammatory diseases caused by various bacterial infections.

• The Journal of the Korean dental association
• /
• v.25 no.1 s.212
• /
• pp.10-10
• /
• 1987

• Proceedings of the PSK Conference
• /
• 2005.11a
• /
• pp.130-130
• /
• 2005

• Journal of Ginseng Research
• /
• v.43 no.2
• /
• pp.163-171
• /
• 2019

Common features of neurodegenerative diseases (NDDs) include progressive dysfunctions and neuronal injuries leading to deterioration in normal brain functions. At present, ginseng is one of the most frequently used natural products. Its use has a long history as a cure for various diseases because its extracts and active compounds exhibit several pharmacological properties against several disorders. However, the pathophysiology of NDDs is not fully clear, but researchers have found that various ion channels and specific signaling pathways might have contributed to the disease pathogenesis. Apart from the different pharmacological potentials, ginseng and its active compounds modulate various ion channels and specific molecular signaling pathways related to the nervous system. Here, we discuss the signal modulating potential of ginseng and its active compounds mainly focusing on those relevant to NDDs.

• Culinary science and hospitality research
• /
• v.23 no.6
• /
• pp.173-183
• /
• 2017

Conditions related to body composition and aging, such as osteopenic obesity, sarcopenia/ sarcopenic obesity, and the newly termed osteosarcopenic obesity(triad of bone, muscle and adipose tissue impairment), are beginning to gain recognition. Currently, it has begun to attract the attention of scholars from all over the world, however, for this disease, it still needs a more clear understanding and perception. Therefore, this article considered the osteoporosis, muscle depression, and obesity, these diseases as a gate to study the relationship among muscle, bone, and fat. In addition, in the aging process, the formation of IGF-cortisol, testosterone, and estrogen is sensitive. These hormones can not only absorb muscle protein metabolism, but also affect alienation. The decrease in IGF-cortisol in the elderly resulted in increased visceral fat, decreased muscle mass and bone mineral density, and then affected decreased skeletal muscle atrophy and decreased quality. The reduction of skeletal muscle quality and strength and increase body fat affected the adipose tissue to produce inflammatory cytokines, thereby reduced skeletal muscle, promoted cardiovascular disease, metabolic syndrome and insulin resistance in chronic diseases. Almost all chronic inflammatory diseases were associated with bone, muscle and fat. These mechanisms were complex and interrelated. Inflammation reduces bone formation, increases fat and reduces muscle mass. And thus not only had a significant impact on the motor system, but also made the incidence increase of fracture, osteoporosis, fragile syndrome, fall, osteomalacia and other bone disease. This article aimed to start from the interaction between the muscles and bones of the elderly, extended to obesity, muscle deficiency, osteoporosis and other diseases, finally, from a nutritional point of view, to discuss how to treat osteoporosis obesity.