• 한국미생물·생명공학회지
• /
• 제45권2호
• /
• pp.110-117
• /
• 2017

본 연구에서는 쌍발이 모자반의 항염증 효과를 알아보기 위해 LPS에 의해 염증반응이 유도된 RAW 264.7 세포에 대한 쌍발이 모자반 에탄올 추출물의 항염증 효과를 살펴보았다. 세포 내 염증매개성 cytokine (IL-6, $TNF-{\alpha}$ 및 $IL-1{\beta}$) 분비량의 경우 농도 의존적인 감소 효과를 보였다. 또한 추출물이 iNOS, COX-2, $NF-{\kappa}B$ 및 MAPKs 발현 억제에 미치는 효과를 알아본 결과, LPS 단독처리구에 의해 각 단백질의 발현량이 현저히 증가하였으나, $50{\mu}g/ml$ 이상의 농도로 추출물을 처리하였을 때 그 발현량이 효과적으로 감소하는 것을 확인할 수가 있었다. 귀 부종 억제 효과 및 조직 관찰을 수행한 결과, 추출물 250 mg/kg 농도에서 prednisolone 50 mg/kg 처리보다 귀 부종이 다소 감소함을 보였으며, 조직관찰 결과 쌍발이 모자반 에탄올 추출물을 처리함으로써 귀 조직의 경피 및 진피 두께가 얇아지고, 조직 내 mast cell 침윤을 현저히 억제함을 보였다. 쌍발이 모자반 에탄올이 보이는 항염증 효과는 해조류 에탄올 추출물 유래 polyphenol 계열의 화합물의 영향이 크다고 생각되며 현재까지 쌍발이 모자반 내의 항염증 효능 물질에 관한 연구는 보고되지 않고 있다. 따라서 본 논문의 결과를 바탕으로 향후 유효성분에 관한 분리 연구가 진행된다면 쌍발이 모자반 에탄올 추출물의 천연 염증 치료 소재로 이용될 가치가 충분할 것으로 사료된다.

• Food Science and Biotechnology
• /
• 제14권4호
• /
• pp.479-486
• /
• 2005

Arabinoxylan, a complex polysaccharide in cereal cell walls, has recently received research attention as a biological response modifier. The immunomodulating effect of arabinoxylans from rice bran (AXrb) was studied using a combined process of extrusion and commercial hemicellulase treatment in order to elucidate the augmentation mechanism of cell-mediated immunity in vitro. The cytotoxicity of mouse spleen lymphocytes against YAC-1 tumor cells was significantly enhanced by treatment with AXrb at $10-100\;{\mu}g/mL$. In an attempt to investigate the mechanism by which AXrb enhance NK cytotoxicity, we examined the effect of AXrb on cytokine production by spleen lymphocytes. Culture supernatants of the cells incubated with AXrb were collected and analyzed for IL-2 and IFN-${\gamma}$ synthesis by ELISA. IL-2 and IFN-${\gamma}$ production were increased significantly. These results suggest that AXrb may induce Th1 immune responses. Macrophages play an important role in host defenses against tumors by killing them and producing secretory products, which protect against bacterial, viral infection and malignant cell growth. AXrb were examined for their ability to induce secretory and cellular responses in murine peritoneal macrophages. When macrophages were treated with various concentrations ($10-100\;{\mu}g/mL$) of AXrb, AXrb induced tumoricidal activity, as well as increasing phagocytosis and the production of NO, $H_2O_2$, TNF-${\alpha}$, IL-$1{\beta}$, and IL-6. These results indicate that reactive oxygen species, reactive nitrogen species, and inflammatory cytokines are likely to be the major mediators of tumoricidal activity in AXrb-treated macrophages. Therefore, AXrb may be useful in cancer immunotherapy and it is anticipated that AXrb obtained using extrusion and subsequent enzyme treatment can be used as an ingredient in nutraceuticals and cereal-based functional food.

• 대한본초학회지
• /
• 제23권2호
• /
• pp.51-58
• /
• 2008

Objectives : Trimellitic anhydride (TMA), a sensitizer that induces occupational asthma and atopic dermatitis, is widely used industrially to make epoxy and alkyd resins, plasticizers, high temperature polymer, and surfactants. The aim of this study was to investigative the effects of aqueous extracts of Lonicera japonica Flower(LJFAE) on TMA-induced contact hypersensitivity (CHS) in Balb/c mice. Methods : The dried flowers of L. japonica were extracted with distilled water at $100^{\circ}C$ for 7 h. The extract was freeze-dried following filteration through 0.45 ${\mu}m$ filter. Mice were orally administrated with or without LJFE of a different doses(25-100 mg/kg) for 28 days. In the challenge period, mice were externally applied at difference doses of LJFAE one time per day 30 min before TMA treatment. We examined the effects of LJFAE on the the serum levels of IgE and prostagladin E2 (PGE2), the Thl/Th2 cytokine production of spleen cells, ear swelling responses, and the leukocyte infiltration induced by TMA. Results : The orally and externally administration of LJFAE dose-dependently reduced the serum levels of IgE and PGE2 production as well as ear swelling responses and leukocyte infiltration in TMA-induced Balb/c mice. Furthermore, the levels of Thl (TNF-${\alpha}$, IFN-${\gammer}$, IL-2)/Th2 (IL-4, IL-5, IL-13) cytokine production from spleen cells stimulated with anti-CD3 and CD28 mAbs was markedly suppressed by the orally and externally treatment with LJFAE in a concentration dependent manner. Conclusions : These results suggest that LJFAE suppresses the inflammatory mediators and regulates the Thl/Th2 cytokines. Therefore, these properties may contribute to the strong anti-CHS response effect of LJFAE.

• 셀메드
• /
• 제4권1호
• /
• pp.3.1-3.8
• /
• 2014

Spa represents a treatment widely used in many rheumatic diseases (RD). The mechanisms by which immersion in mineral or thermal water ameliorates RD are not fully understood. The net benefit is probably the result of a combination of factors, among which the mechanical, thermal and chemical effects are most prominent. Buoyancy, immersion, resistance and temperature play important roles. According to the gate theory, pain relief may be due to the pressure and temperature of the water on skin; heat may reduce muscle spasm and increase the pain threshold. Mud-bath therapy increases plasma ${\beta}$-endorphin levels and secretion of corticotrophin, cortisol, growth hormone and prolactin. It has recently been demonstrated that thermal mud-bath therapy induces a reduction in circulating levels of prostaglandin E2, leukotriene B4, interleukin-$1{\beta}$ and tumour necrosis factor-${\alpha}$, important mediators of inflammation and pain. Furthermore, balneotherapy has been found to cause an increase in insulin-like growth factor-1, which stimulates cartilage metabolism, and transforming growth factor-${\beta}$. Beneficial anti-inflammatory and anti-degenerative effects of mineral water were confirmed in chondrocytes cultures, too. Various studies in vitro and in humans have highlighted the positive action of mud-packs and thermal baths, especially sulphurous ones, on the oxidant/antioxidant system. Overall, thermal stress has an immunosuppressive effect. Many other non-specific factors may also contribute to the beneficial effects observed after spa therapy in some RD, including effects on cardiovascular risk factors (e.g. adipokines) and changes in the environment, pleasant surroundings and the absence of work duties.

• Restorative Dentistry and Endodontics
• /
• 제24권1호
• /
• pp.187-199
• /
• 1999

Bone remodeling is characterized by the continuing processes of osteoblast-mediated bone formation and osteoclast-mediated bone resorption. Bone metabolism is tightly regulated at the local level by networks of hormones, cytokines, and other factors. In pathological conditions of bone remodeling, including osteoporosis and periodontal diseases, inflammatory cytokines and local mediators are responsible for enhancement of osteoclast resorption and inhibition of repair at the sites of bone resorption. TNF-${\alpha}$ is a pleiotropic hormone with actions on the differentiation, growth, and functional activities of normal and malignant cells from numerous tissues. TNF-${\alpha}$ has been proposed as a local mediator of the control of bone turnover in situations of chronic inflammation, and it has been assumed that the local source of TNF-${\alpha}$ is the monocyte in the adjacent bone marrow or the local circulation. TNF-${\alpha}$ is a potent inducer of bone resorption. TNF-${\alpha}$ is known to induce the activation of apoptotic signaling pathway, which leads to the apoptosis of bone cells. We demonstrated that treatment of murine osteoblastic MC3T3E1 cells with TNF-${\alpha}$ decreases proliferation as well as alkaline phosphatase (ALP) activity in a dose depenent manner. In addition, TNF-${\alpha}$ increases osteoclast-like cell formation in $1{\alpha}$, 25(OH)2D3 or PGE2-treated bone marrow cell culture. When cells were cultured in TNF-${\alpha}$ free ${\alpha}$-MEM, this inhibitory effect of ALP activity was reversible up to 10 ng/ml TNF-${\alpha}$, in contrast, at the 20 ng/ml TNF-${\alpha}$, irreversible. In this concentration, TNF-${\alpha}$ may induce apoptosis in MC3T3E1 cells. In this study, TNF-${\alpha}$ induces apoptosis resulting in chromosomal DNA fragmentation, preceded by JNK/SAPKs and caspase-3 activation. Our present results show that JNK/SAPKs and caspase-3 are activated by TNF-${\alpha}$, suggesting that the JNK/SAPKs and caspase-3 participate in the bone resorption, associated with apoptosis.

• The Korean Journal of Physiology and Pharmacology
• /
• 제1권2호
• /
• pp.201-208
• /
• 1997

It is becoming increasingly clear that the inflammatory reaction can be ascribed to a complex array of mediators generated and released from activated phagocytes. In this study, the effect of PAF on interleukin-1(IL-1) activity by rat alveolar macrophages(AM) was examined using thymocyte proliferation assay in the supernate of sample obtained after 24 hr culture. When AM were cultured with PAF alone, no change in IL-1 activity was observed. However, the combined addition of PAF and muramyl dipeptide(MDP) or lipopolysaccharide(LPS) to AM cultures markedly enhanced IL-1 activity by 2-3 fold compared with AM cultures with the stimulant alone in a concentration dependent fashion. The peack effect was found at $10^{-8}$ M PAF with MDP and $10^{-14}$ M PAF with LPS. the effect of PAF was also tested in silica, toxic respirable dust, -added AM cultures as well as in the cultures containing bacterial compounds. Although silica did not stimulate the IL-1 activity, PAF could enhance IL-1 activity by 2 fold above the value of the silica-treated AM cultures with the peak response at $10^{-12}$ M PAF. Optimal enhancement of IL-1 activity occured when MDP and PAF were present together at the initiation of the 24 hr AM cultures. Additionaly, the biologically inactive precursor/metabolite of PAF, lyso-PAF failed to induce enhancement of IL-1 activity. When the specific, but structurally different PAF receptor antagonists, BN 52021($10^{-5}$ M) and CV 3988($10^{-5}$ M) was treated 15 min before addition of PAF($10^{-8}$ M) and MDP$(10\;{\mu}g/ml)$ to the AM cultures, it markedly inhibited the enhancement of IL-1 activity induced by PAF. The effects of these PAF antagonists were also observed in LPS$(10\;{\mu}g/ml)$-stimulated cells. Collectively, these data suggest that PAF enhances IL-1 activity by interaction with a specific receptor.

• The Korean Journal of Physiology and Pharmacology
• /
• 제21권1호
• /
• pp.1-9
• /
• 2017

Intestinal disorders often co-occur with inflammation and dysmotility. However, drugs which simultaneously improve intestinal inflammation and co-occurring dysmotility are rarely reported. Atractylodin, a widely used herbal medicine, is used to treat digestive disorders. The present study was designed to characterize the effects of atractylodin on amelioration of both jejunal inflammation and the co-occurring dysmotility in both constipation-prominent (CP) and diarrhea-prominent (DP) rats. The results indicated that atractylodin reduced proinflammatory cytokines TNF-${\alpha}$, IL-$1{\beta}$, and IL-6 in the plasma and inhibited the expression of inflammatory mediators iNOS and NF-kappa B in jejunal segments in both CP and DP rats. The results indicated that atractylodin exerted stimulatory effects and inhibitory effects on the contractility of jejunal segments isolated from CP and DP rats respectively, showing a contractile-state-dependent regulation. Atractylodin-induced contractile-state-dependent regulation was also observed by using rat jejunal segments in low and high contractile states respectively (5 pairs of low/high contractile states). Atractylodin up-regulated the decreased phosphorylation of 20 kDa myosin light chain, protein contents of myosin light chain kinase (MLCK), and MLCK mRNA expression in jejunal segments of CP rats and down-regulated those increased parameters in DP rats. Taken together, atractylodin alleviated rat jejunal inflammation and exerted contractile-state-dependent regulation on the contractility of jejunal segments isolated from CP and DP rats respectively, suggesting the potential clinical implication for ameliorating intestinal inflammation and co-occurring dysmotility.

• 한방안이비인후피부과학회지
• /
• 제24권1호
• /
• pp.64-77
• /
• 2011

Objectives : 판람근(板藍根)은 십자화과에 속하는 대청(大靑) 또는 숭남의 근(根)을 건조한 것이다. 본 연구는 판람근(板藍根)이 청열해독(淸熱解毒)함에 근거하여, LPS로 활성화된 Raw264.7 cell에서 판람근(板藍根)과 그 성분중의 하나인 tryptanthrin이 염증매개물질에 미치는 효과를 살펴보고자 하였다. Methods : 세포생존율은 MTT, nitric oxide (NO)는 Griess reagent를 사용하여 측정하였으며, 각 단백질의 발현량은 Western blot 방법을 사용하였으며, cytokine 및 cyclooxygenase-2 (COX-2)는 ELISA방법을 사용하여 측정하였다. Results : LPS는 NO 및 prostaglandin E2 (PGE2)를 유의하게 상승시켰으며, 판람근(板藍根)추출물 (IRE) 및 tryptanthrin 은 이들을 유의하게 억제하였다. 그러나 판람근(板藍根)의 또 다른 성분인 indigo는 유의한 결과를 나타내지 못하였다. IRE와 tryptanthrin은 inhibitory kappa B alpha의 인산화를 억제하여, nuclear factor-${\kappa}$B (NF-${\kappa}$B)의 핵으로의 전위(轉位)를 억제하여, iNOS 및 cytokine을 억제하였다. IRE와 tryptanthrin의 PGE2 억제는, COX-2의 발현억제에서가 아니라, COX-2의 활성을 억제함에서 기인하였다. Conclusion : 이러한 결과는 판람근(板藍根)이 NF-${\kappa}$B pathway를 경유하여 iNOS의 발현 및 COX-2의 활성을 억제함을 나타내며, 이러한 판람근(板藍根)의 항염증효능은 일부 tryptanthrin의 작용에서 기인함을 시사한다.

• International Journal of Industrial Entomology and Biomaterials
• /
• 제35권1호
• /
• pp.14-21
• /
• 2017

Gastric ulcer is a clinical symptom characterized by inflammation of the gastric mucosa. Stress and alcohol consumption have been identified as the major cause of gastric ulcer. However, the effects of silkworms on ethanol-induced gastric ulcer have not been studied yet. The mature silkworms that are difficult to eat have become easier to ingest due to recent technological development to make steaming and freeze-drying mature silkworm larval powder (SMSP). In this study, we investigated whether three silkworm varieties, Baekokjam, Golden-silk and Yeonnokjam could alleviate ethanol-induced gastric mucosal damage in vivo. Sprague-Dawley rats pretreated with 3 SMSPs (0.1 or 1 g/kg BW) or normal diet (AIN-76A) were exposed to absolute ethanol (3 g/kg BW, 3 h) by oral gavage. Morphological examination included ulcer index as a measurement of hemorrhages and hematoxylin and eosin staining was performed to analyze the severity of gastric ulcer. Results of macroscopic examination suggested that all 3 SMSPs pretreatment significantly protected gastric mucosa against ethanol-induced damage. Microscopic observations demonstrated significant mucosal erosion and inflammation in ethanol-treated rats, which was abrogated in rats pretreated with 3 SMSPs. In addition, pretreatment with all 3 SMSPs showed significant decreases the expression of pro-inflammatory mediators, IL-6 and cyclooxygenase-2. Among SMSP from 3 varieties of silkworm, preadministration of 1 g/kg Baekokjam SMSP showed the most effective protective effect against ethanol-induced gastric ulcer. These results suggest that Baekokjam SMSP can be a potential gastroprotective agent against ethanol-induced gastric ulcer.

• IMMUNE NETWORK
• /
• 제12권3호
• /
• pp.113-117
• /
• 2012

FasL, perforin, $TNF{\alpha}$, IL-1 and NO have been considered as effector molecule(s) leading to ${\beta}$-cell death in autoimmune diabetes. However, the real culprit(s) of ${\beta}$-cell destruction have long been elusive despite intense investigation. Previously we have suggested $IFN{\gamma}/TNF{\alpha}$ synergism as the final effector molecules in autoimmune diabetes of NOD mice. A combination of $IFN{\gamma}$ and $TNF{\alpha}$ but neither cytokine alone, induced classical caspase-dependent apoptosis in murine insulinoma and pancreatic islet cells. $IFN{\gamma}$ treatment conferred susceptibility to $TNF{\alpha}$-induced apoptosis on otherwise resistant murine insulinoma cells by STAT1 activation followed by IRF-1 induction. Here we report that $IFN{\gamma}/TNF{\alpha}$ synergism induces apoptosis of human pancreatic islet cells. We also observed STAT1 activation followed by IRF-1 induction by $IFN{\gamma}$ treatment in human islet cells. Taken together, we suggest that $IFN{\gamma}/TNF{\alpha}$ synergism could be involved in human islet cell death in type 1 diabetes, similar to murine type 1 diabetes.