• 한국독성학회:학술대회논문집
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• 한국독성학회 2001년도 International Symposium on Dietary and Medicinal Antimutgens and Anticarcinogens
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• pp.27-27
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• 2001

Significant evidence exists which demonstrates that inflammation predisposes and promotes the cancer process in humans. Chronic inflammation can induce cancer in a variety of organ sites, including bowel and lung. There is also firm evidence that induced cyclooxygenases and nitric oxide synthetases, prostaglandins, and inflammatory cytokines can promote and accelerate the carcinogenic process.(omitted)

• Annals of Clinical Neurophysiology
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• 제22권2호
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• pp.129-130
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• 2020

• The Korean Journal of Pain
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• 제35권4호
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• pp.488-488
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• 2022

• International Journal of Oral Biology
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• 제41권3호
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• pp.125-131
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• 2016

The aim of the present study was to develop an animal model for evaluation of temporomandibular (TMJ) nociception under TMJ inflammation. We also investigated the participation of $IL-1{\beta}$ in inflammation-induced TMJ nociception. Experiments were carried out using male Sprague-Dawley rats. Intra-articular injection of 3% formalin was administered to evaluate hyperalgesia 3 days after CFA injection. Intra-articular injection of 3% formalin did not produce nociceptive behavior in normal rats. Although intra-articular injection of 3 doses of CFA produced TMJ inflammation, only 1:3 diluted CFA produced hyperalgesia when formalin was injected intra-articularly 3 days after CFA injection. Co-administration of IL-1 receptor inhibitor with formalin into the TMJ cavity 3 days after CFA injection was performed. Co-administration of IL-1 receptor inhibitor significantly inhibited formalin-induced hyperalgesia in rats with CFA-induced TMJ inflammation. These results suggested that intra-articular injection of formalin produced hyperalgesia under chronic TMJ inflammation. Moreover, $IL-1{\beta}$ plays an important role in TMJ hyperalgesia under chronic inflammation and blockade of $IL-1{\beta}$ is a potential therapeutic target for inflammatory TMJ pain.

• BMB Reports
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• 제47권1호
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• pp.1-7
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• 2014

Atherosclerosis is a pathologic process occurring within the artery, in which many cell types, including T cell, macrophages, endothelial cells, and smooth muscle cells, interact, and cause chronic inflammation, in response to various inner- or outer-cellular stimuli. Atherosclerosis is characterized by a complex interaction of inflammation, lipid deposition, vascular smooth muscle cell proliferation, endothelial dysfunction, and extracellular matrix remodeling, which will result in the formation of an intimal plaque. Although the regulation and function of vascular smooth muscle cells are important in the progression of atherosclerosis, the roles of smooth muscle cells in regulating vascular inflammation are rarely focused upon, compared to those of endothelial cells or inflammatory cells. Therefore, in this review, we will discuss here how smooth muscle cells contribute or regulate the inflammatory reaction in the progression of atherosclerosis, especially in the context of the activation of various membrane receptors, and how they may regulate vascular inflammation.

• 한국해양바이오학회지
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• 제2권2호
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• pp.86-93
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• 2007

만성염증은 치주염, 대장염, 간염 및 관절염과 밀접한 관련성이 있다고 알려져 있다. 최근에 항염증제가 해양자원으로부터 개발되고 있다. 본 연구에서는 감태 (EC)가 항염증효과가 있다는 것이 발견되었다. 갈조류에 속하는 감태의 에탄올 추출물이 RAW 264.7 세포에서 tumor necrosis factor-${\alpha}$ interleukin-$1{\beta}$, interleukin-6 and prostaglandin $E_2$와 같은 염증매개체의 생성에 탁월한 효과를 나타내었다. 더욱이 reporter gene assay 및 western blot 분석 에 서 감태추출물은 대식세포에서 염증매개체의 발현을 조절하는 NF-${\kappa}B$ 전사인자의 불활성화를 통하여 항염증효과를 나타내었다. 뿐만 아니라 감태추출물은 만성염증에 중요한 역할을 하는 기질금속단백질의 활성을 억제 하였다. 이러한 결과는 갑태추출물이 만성염증을 억제하는데 잠재적으로 이용될 수 있다는 것을 암시하고 있다.

• Journal of Microbiology and Biotechnology
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• 제33권5호
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• pp.634-643
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• 2023

Chronic obstructive pulmonary disease (COPD), one of the leading causes of death worldwide, is caused by repeated exposure to harmful matter, such as cigarette smoke. Although Lilium longiflorum Thunb (LLT) has anti-inflammatory effects, there is no report on the fermented LLT bulb extract regulating lung inflammation in COPD. Thus, we investigated the protective effect of LLT bulb extract fermented with Lactobacillus acidophilus 803 in COPD mouse models induced by cigarette smoke extract (CSE) and porcine pancreas elastase (PPE). Oral administration of the fermented product (LS803) suppressed the production of inflammatory mediators and the infiltration of immune cells involving neutrophils and macrophages, resulting in protective effects against lung damage. In addition, LS803 inhibited CSE- and LPS-induced IL-6 and IL-8 production in airway epithelial H292 cells as well as suppressed PMA-induced formation of neutrophil extracellular traps in HL-60 cells. In particular, LS803 significantly repressed the elevated IL-6 and MIP-2 production after CSE and LPS stimulation by suppressing the activity of the nuclear factor kappa-light-chain-enhancer of activated B (NFκB) in mouse peritoneal macrophages. Therefore, our results suggest that the fermented product LS803 is effective in preventing and alleviating lung inflammation.

• Journal of Microbiology and Biotechnology
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• 제33권9호
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• pp.1111-1118
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• 2023

As a long-term condition that affects the airways and lungs, chronic obstructive pulmonary disease (COPD) is characterized by inflammation, emphysema, breathlessness, chronic cough, and sputum production. Currently, the bronchodilators and anti-inflammatory drugs prescribed for COPD are mostly off-target, warranting new disease management strategies. Accumulating research has revealed the gut-lung axis to be a bidirectional communication system. Cigarette smoke, a major exacerbating factor in COPD and lung inflammation, affects gut microbiota composition and diversity, causing gut microbiota dysbiosis, a condition that has recently been described in COPD patients and animal models. For this review, we focused on the gut-lung axis, which is influenced by gut microbial metabolites, bacterial translocation, and immune cell modulation. Further, we have summarized the findings of preclinical and clinical studies on the association between gut microbiota and COPD to provide a basis for using gut microbiota in therapeutic strategies against COPD. Our review also proposes that further research on probiotics, prebiotics, short-chain fatty acids, and fecal microbiota transplantation could assist therapeutic approaches targeting the gut microbiota to alleviate COPD.

• 생약학회지
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• 제25권2호
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• pp.153-159
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• 1994

The studies were conducted to investigate the inflammation, gastric ulcer, analgesic and homothrmic of experimental animals by KYUNG OK-KO water extract and drink, which is a traditional preparation in Korea. 1. It was exhibited significantly anti-inflammatory effects to acute inflammation on carragennan edema, and preventive and therapeutic effects to chronic inflammation on Freund's complete adjuvant in rats(100, 200, 400 mg/kg). Especially, preventive effect of KYUNG OK-KO water extracts at doses of 100, 200, 400 mg/kg in rats were showed dose-dependantly. 2. Aspirin-induced gastric ulcer were remarkably repaired by all experimental groups of KYUNG OK-KO water extracts. 3. The number of writing syndromes by acetic acid induced also were decreased which MPI's test was increased by tail flick apparatus in mice remarkably, all doses of water extracts(100, 200, 400 mg/kg) and dose-dependantly. 4. Aminopyrine-induced homothermic effects of KYUNG OK-KO water extract(100, 200, 400mg/kg) and drink (0.7, 1.4, 2.1 ml/kg) were significantly evaluated dose-dependantly in 400 mg/kg, 2.1 ml/kg groups.

• Asian Pacific Journal of Cancer Prevention
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• 제16권10호
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• pp.4161-4168
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• 2015

Colorectal cancer (CRC) is a worldwide health problem, being the third most commonly detected cancer in males and the second in females. Rising CRC incidence trends are mainly regarded as a part of the rapid 'Westernization' of life-style and are associated with calorically excessive high-fat/low-fibre diet, consumption of refined products, lack of physical activity, and obesity. Most recent epidemiological and clinical investigations have consistently evidenced a significant relationship between obesity-driven inflammation in particular steps of colorectal cancer development, including initiation, promotion, progression, and metastasis. Inflammation in obesity occurs by several mechanisms. Roles of imbalanced metabolism (MetS), distinct immune cells, cytokines, and other immune mediators have been suggested in the inflammatory processes. Critical mechanisms are accounted to proinflammatory cytokines (e.g. IL-1, IL-6, IL-8) and tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$). These molecules are secreted by macrophages and are considered as major agents in the transition between acute and chronic inflammation and inflammation-related CRC. The second factor promoting the CRC development in obese individuals is altered adipokine concentrations (leptin and adiponectin). The role of leptin and adiponectin in cancer cell proliferation, invasion, and metastasis is attributable to the activation of several signal transduction pathways (JAK/STAT, mitogen-activated protein kinase (MAPK), phosphatidylinositol 3 kinase (PI3K), mTOR, and 5'AMPK signaling pathways) and multiple dysregulation (COX-2 downregulation, mRNA expression).