• Biomolecules & Therapeutics
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• v.15 no.1
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• pp.7-15
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• 2007

There have been various animal models of skin inflammation. These models have been used for establishing anti-inflammatory activity of the topical agents including cosmetics. Here, the molecular mechanisms of most widely-used animal models of skin inflammation including contact irritation, acute and chronic inflammation, and delayed-type hypersensitivity are summarized. Against these animal models, varieties of plant flavonoids showed anti-inflammatory activity. The action mechanisms of anti-inflammation by topical flavonoids are presented. A therapeutic potential of flavonoids is discussed.

• CELLMED
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• v.12 no.5
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• pp.3.1-3.3
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• 2022

Objective: A Case Report on Reduction of Inflammation Using Nutritional Therapy Methods: The patient is a Korean male aged 62 years. The wound has developed inflammation and is not healing while the patient complains of pain. Results: After nutritional therapy, inflammation diminished. Conclusion: Nutritional therapy can be beneficial for inflammation, for which even skin transplantation was advised.

• The Korean Journal of Physiology
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• v.23 no.1
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• pp.151-167
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• 1989

The present study was undertaken to investigate modification in electrophysiological characteristics of cat dorsal horn cells resulting from carrageenin-induced inflammation. The followings were studied; 1) the time-course of changes in responses of the WDR (wide dynamic range) cell 1-3h after subcutaneous injection of carrageenin in its receptive field; 2) the responses of the same dorsal hern cells before and after induction of inflammation; 3) the effect of inflammation on the responsiveness of dorsal horn neurons to algogens (bradykinin & potassium); and 4) the effect of inflammation on the activity of WDR cell following administration of indomethacin and clonidine. Though responses of WDR neuron were increased dramatically during first 1h, the maximal enhancement was observed 3h after induction of inflammation especially by repetitive light tactile stimulus. Following carrageenin injection the majority of WDR neurons (10/15 units) showed enhanced responses to all the mechanical stimuli while in 3 cases responsiveness were intensified during activation by one tactile stimulus (brush or pressure). One cell was unaffected by inflammation and in another case the response was enhanced only to noxious stimulus. Five of 9 cells that could initially be driven by noxious stimulus were activated more strongly by same stimulus and even by tactile stimulus (pressure) following inflammation. In 2 cases neurons were sensitized only to noxious stimulus whereas in another 2 cells that did not show enhanced responses to noxious stimulus responses to light tactile stimulus (pressure) appeared after inflammation. Of 16 LT cells tested 6 responded to squeeze while 4 showed the characteristics of WDR cell following inflammation. No modification in responsiveness was recognized in 3 cells whereas response to only brush was enhanced in another 3 neurons. Following carrageenin injection responses of LT cell to bradykinin or $K^{+}$ were not altered whereas those of WOR neurons to bradykinin or $K^{+}$ were suppressed in 22.2% and 33.3% of cases, respectively. In two of 8 activity of HT cells were inhibited by bradykinin while in five of 8 responsiveness to $K^{+}$ were rather enhanced by inflammation. In the rest inflammation was ineffective. In inflammation-induced animal the receptive field of LT cell was not changed whereas those of WDR cell and HT cell were tremendously expanded. The enhanced responses of WDR neurons to mechanical stimuli resulted from inflammation were suppressed by intravenously injected indomethacin and clonidine suggesting that postaglandin is involved in inflammation-induced sensitization of these cells. The involvement of peripheral and central mechanisms in the modification in responsiveness of dorsal horn cells in the carrageenin-induced inflammation was discussed.

• Journal of Ginseng Research
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• v.42 no.1
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• pp.68-74
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• 2018

Background: Ginsenosides have been reported to have many health benefits, including anti-inflammatory effects, and the resolution of inflammation is now considered to be an active process driven by M2-type macrophages. In order to determine whether ginsenosides modulate macrophage phenotypes to reduce inflammation, 11 ginsenosides were studied with respect to macrophage polarization and the resolution of inflammation. Methods: Mouse peritoneal macrophages were polarized into M1 or M2 phenotypes. Reverse transcription-polymerase chain reaction, Western blotting, and measurement of nitric oxide (NO) and prostaglandin $E_2$ levels were performed in vitro and in a zymosan-induced peritonitis C57BL/6 mouse model. Results: Ginsenoside $Rg_3$ was identified as a proresolving ginseng compound based on the induction of M2 macrophage polarization. Ginsenoside $Rg_3$ not only induced the expression of arginase-1 (a representative M2 marker gene), but also suppressed M1 marker genes, such as inducible NO synthase, and NO levels. The proresolving activity of ginsenoside $Rg_3$ was also observed in vivo in a zymosan-induced peritonitis model. Ginsenoside $Rg_3$ accelerated the resolution process when administered at peak inflammatory response into the peritoneal cavity. Conclusion: These results suggest that ginsenoside $Rg_3$ induces the M2 polarization of macrophages and accelerates the resolution of inflammation. This finding opens a new avenue in ginseng pharmacology.

• Nutrition Research and Practice
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• v.8 no.3
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• pp.233-240
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• 2014

Epidemiology studies indicate that diet or specific dietary components can reduce the risk for cancer, cardiovascular disease and diabetes. An underlying cause of these diseases is chronic inflammation. Dietary components that are beneficial against disease seem to have multiple mechanisms of action and many also have a common mechanism of reducing inflammation, often via the $NF{\kappa}B$ pathway. Thus, a plant based diet can contain many components that reduce inflammation and can reduce the risk for developing all three of these chronic diseases. We summarize dietary components that have been shown to reduce cancer risk and two studies that show that dietary walnut can reduce cancer growth and development. Part of the mechanism for the anticancer benefit of walnut was by suppressing the activation of $NF{\kappa}B$. In this brief review, we focus on reduction of cancer risk by dietary components and the relationship to suppression of inflammation. However, it should be remembered that most dietary components have multiple beneficial mechanisms of action that can be additive and that suppression of chronic inflammation should reduce the risk for all three chronic diseases.

• The Korean Journal of Pain
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• v.35 no.4
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• pp.488-488
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• 2022

• IMMUNE NETWORK
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• v.9 no.1
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• pp.8-11
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• 2009

There is mounting evidence that autophagy is involved in diverse physiological and pathological processes that have immense relevance in human development, diseases and aging. Immunity and inflammation are not exceptions. Here, the role of autophagy in the control of immune processes particularly that related to cell death and inflammation is discussed.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.175-176
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• 2002

Airway inflammation is a characteristic of many lung disorders including asthma, chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis. All these diseases involve the recruitment of immune and inflammatory cells to the lungs leading to systemic and local chronic inflammation and oxidative stress. (omitted)

• Molecules and Cells
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• v.43 no.5
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• pp.431-437
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• 2020

The hypothalamus is a crucial organ for the maintenance of appropriate body fat storage. Neurons in the hypothalamic arcuate nucleus (ARH) detect energy shortage or surplus via the circulating concentrations of metabolic hormones and nutrients, and then coordinate energy intake and expenditure to maintain energy homeostasis. Malfunction or loss of hypothalamic ARH neurons results in obesity. Accumulated evidence suggests that hypothalamic inflammation is a key pathological mechanism that links chronic overconsumption of a high-fat diet (HFD) with the development of obesity and related metabolic complications. Interestingly, overnutrition-induced hypothalamic inflammation occurs specifically in the ARH, where microglia initiate an inflammatory response by releasing proinflammatory cytokines and chemokines in response to excessive fatty acid flux. Upon more prolonged HFD consumption, astrocytes and perivascular macrophages become involved and sustain hypothalamic inflammation. ARH neurons are victims of hypothalamic inflammation, but they may actively participate in hypothalamic inflammation by sending quiescence or stress signals to surrounding glia. In this mini-review, we describe the current state of knowledge regarding the contributions of neurons and glia, and their interactions, to HFD-induced hypothalamic inflammation.

• IMMUNE NETWORK
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• v.14 no.5
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• pp.249-254
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• 2014

Allergic asthma is a chronic pulmonary inflammatory disease characterized by reversible airway obstruction, hyperresponsiveness and eosinophils infiltration. Toll-like receptors (TLRs) signaling are closely associated with asthma and have emerged as a novel therapeutic target in allergic disease. The functions of TLR3 and TLR4 in allergic airway inflammation have been studied; however, the precise role of TIR-domain-containing adapter-inducing interferon-${\beta}$ (TRIF), the adaptor molecule for both TLR3 and TLR4, is not yet fully understood. To investigate this, we developed a mouse model of OVA-induced allergic airway inflammation and compared the severity of allergic airway inflammation in WT and $TRIF^-/^-$ mice. Histopathological assessment revealed that the severity of inflammation in airway inflammation in TRIF-deficient mice was comparable to that in WT mice. The total number of cells recovered from bronchoalveolar lavage fluid did not differ between WT and TRIF-deficient mice. Moreover, TRIF deficiency did not affect Th1 and Th2 cytokine production in lung tissue nor the level of serum OVA-specific IgE, $IgG_1$ and $IgG_{2c}$. These findings suggest that TRIF-mediated signaling may not be critical for the development of allergic airway inflammation.