• Nutrition Research and Practice
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• v.9 no.6
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• pp.619-627
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• 2015

BACKGROUND/OBJECTIVES: Colitis is a serious health problem, and chronic obesity is associated with the progression of colitis. The aim of this study was to determine the effects of natural raw meal (NRM) on high-fat diet (HFD, 45%) and dextran sulfate sodium (DSS, 2% w/v)-induced colitis in C57BL/6J mice. MATERIALS/METHODS: Body weight, colon length, and colon weight-to-length ratio, were measured directly. Serum levels of obesity-related biomarkers, triglyceride (TG), total cholesterol (TC), low density lipoprotein (LDL), high density lipoprotein (HDL), insulin, leptin, and adiponectin were determined using commercial kits. Serum levels of pro-inflammatory cytokines including tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), interleukin (IL)-$1{\beta}$, and IL-6 were detected using a commercial ELISA kit. Histological study was performed using a hematoxylin and eosin (H&E) staining assay. Colonic mRNA expressions of TNF-${\alpha}$, IL-$1{\beta}$, IL-6, inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) were determined by RT-PCR assay. RESULTS: Body weight and obesity-related biomarkers (TG, TC, LDL, HDL, insulin, leptin, and adiponectin) were regulated and obesity was prevented in NRM treated mice. NRM significantly suppressed colon shortening and reduced colon weight-to-length ratio in HFD+DSS induced colitis in C57BL/6J mice (P < 0.05). Histological observations suggested that NRM reduced edema, mucosal damage, and the loss of crypts induced by HFD and DSS. In addition, NRM decreased the serum levels of pro-inflammatory cytokines, TNF-${\alpha}$, IL-$1{\beta}$, and IL-6 and inhibited the mRNA expressions of these cytokines, and iNOS and COX-2 in colon mucosa (P < 0.05). CONCLUSION: The results suggest that NRM has an anti-inflammatory effect against HFD and DSS-induced colitis in mice, and that these effects are due to the amelioration of HFD and/or DSS-induced inflammatory reactions.

• The Korea Journal of Herbology
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• v.39 no.1
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• pp.31-38
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• 2024

Objectives : Ulcerative colitis is a chronic recurrent inflammatory disease of the gastrointestinal tract. However, there are some drawbacks to long-term drug therapy such as the risk of opportunistic infections. Recently, there was an increasing interest on the use of khorasan Kamut wheat because of their higher value of selenium and fiber than modern wheat. The present study was aimed to investigate the effect of Kamut brand wheat enzyme (Kamut WE) diet on colon health in dextran sulfate sodium (DSS)-induced colitis mice. Methods : Female C57BL/6J mice were divided into 6 groups. (1) normal (Water and AIN-93G diet), (2) control (1.25% DSS and AIN-93G diet), (3) Kamut WE (1.25% DSS and Kamut WE diet), (4) normal (Water and AIN-93G diet), (5) control (2.50% DSS and AIN-93G diet), (6) Kamut WE (2.50% DSS and Kamut WE diet). Dietary intake, body weight change, disease activity index (DAI), colon length and spleen weight were monitored. Results : Kamut WE group alleviated colitis symptom, including dietary intake loss, DAI (weight loss, loose stools, bleeding), colon length shortening and spleen swelling. Further, Kamut WE diets showed a significant effect against pathological damage by the increased colon length, decreased DAI and spleen weight in DSS 1.25% as well as DSS 2.50%. Conclusions : Our study provides evidence that Kamut WE diet increased colon length, decreased DAI and spleen weight in intestinal inflammation.

• Journal of Ginseng Research
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• v.42 no.1
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• pp.50-56
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• 2018

Background: Saponins from Panax japonicus (SPJ) are the most abundant and main active components of P. japonicus, which replaces ginseng roots in treatment for many kinds of diseases in the minority ethnic group in China. Our previous studies have demonstrated that SPJ has the effects of anti-inflammation through the mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-${\kappa}B$) signaling pathways. The present study was designed to investigate whether SPJ can modulate intestinal tight junction barrier in aging rats and further to explore the potential mechanism. Methods: Aging rats had been treated with different doses (10 mg/kg, 30 mg/kg, and 60 mg/kg) of SPJ for 6 mo since they were 18 mo old. After the rats were euthanized, the colonic samples were harvested. Levels of tight junctions (claudin-1 and occludin) were determined by immunohistochemical staining. Levels of proinflammatory cytokines (interleukin-$1{\beta}$ and tumor necrosis factor-${\alpha}$) were examined by Western blot. NF-${\kappa}B$ and phosphorylation of MAPK signaling pathways were also determined by Western blot. Results: We found that SPJ increased the expression of the tight junction proteins claudin-1 and occludin in the colon of aging rats. Treatment with SPJ decreased the levels of interleukin-$1{\beta}$ and tumor necrosis factor-${\alpha}$, reduced the phosphorylation of three MAPK isoforms, and inhibited the expression of NF-${\kappa}B$ in the colon of aging rats. Conclusion: The studies demonstrated that SPJ modulates the damage of intestinal epithelial tight junction in aging rats, inhibits inflammation, and downregulates the phosphorylation of the MAPK and $NF-{\kappa}B$ signaling pathways.

• Biomolecules & Therapeutics
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• v.27 no.1
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• pp.1-14
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• 2019

Resveratrol was first isolated in 1939 by Takaoka from Veratrum grandiflorum O. Loes. Following this discovery, sporadic descriptive reports appeared in the literature. However, spurred by our seminal paper published nearly 60 years later, resveratrol became a household word and the subject of extensive investigation. Now, in addition to appearing in over 20,000 research papers, resveratrol has inspired monographs, conferences, symposia, patents, chemical derivatives, etc. In addition, dietary supplements are marketed under various tradenames. Once resveratrol was brought to the limelight, early research tended to focus on pharmacological activities related to the cardiovascular system, inflammation, and cancer but, over the years, the horizon greatly expanded. Around 130 human clinical trials have been (or are being) conducted with varying results. This may be due to factors such as disparate doses (ca. 5 to 5,000 mg/day) and variable experimental settings. Further, molecular targets are numerous and a dominant mechanism is elusive or nonexistent. In this context, the compound is overtly promiscuous. Nonetheless, since the safety profile is pristine, and use as a dietary supplement is prevalent, these features are not viewed as detrimental. Given the ongoing history of resveratrol, it is reasonable to advocate for additional development and further clinical investigation. Topical preparations seem especially promising, as do conditions that can respond to anti-inflammatory action and/or direct exposure, such as colon cancer prevention. Although the ultimate fate of resveratrol remains an open question, thus far, the compound has inspired innovative scientific concepts and enhanced public awareness of preventative health care.

• The Journal of Pediatrics of Korean Medicine
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• v.35 no.1
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• pp.30-39
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• 2021

Objective The purpose of this study is to learn the anti-inflammatory effect of Douchi on ulcerative colitis (UC). Methods Three-month-old mice were divided into 4 groups as follows: control group (Ctrl), UC induced group (UCEG), Pentasa treated group after inducing UC (OPTG), and Douchi treated group after inducing UC (FGTG). NF-κB, p-IκB, iNOS, COX-2 were observed by immunohistochemistry and Masson trichrome, PAS, and Phloxine-tartrazine staining were used to observe histochemical changes. Results Inflammation indicators of the large intestine were significantly lower in FGTG than in the UCEG and OPTG. Also, indicators involved in pulmonary alveolar formation were significantly higher in the FGTG than in the UCEG and OPTG. Conclusions The result of this study suggests that Douchi extract was effective in ulcerative colitis and helped in the formation of alveolar. This result suggests that the lungs and colon are correlated.

• Parasites, Hosts and Diseases
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• v.50 no.4
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• pp.385-390
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• 2012

In order to know the effect of pre-existing Trichinella spiralis infection on experimentally induced intestinal inflammation and immune responses, we induced colitis in T. spiralis-infected mice and observed the severity of colitis and the levels of Th1, Th2, and regulatory cytokines and recruitment of $CD4^+CD25^+Foxp3^+$ T (regulatory T; $T_{reg}$) cells. Female C57BL/6 mice were infected with 250 muscle larvae; after 4 weeks, induction of experimental colitis was performed using 3% dextran sulfate sodium (DSS). During the induction period, we observed severity of colitis, including weight loss and status of stool, and evaluated the disease activity index (DAI). A significantly low DAI and degree of weight loss were observed in infected mice, compared with uninfected mice. In addition, colon length in infected mice was not contracted, compared with uninfected mice. We also observed a significant increase in production of pro-inflammatory cytokines, IL-6 and IFN-${\gamma}$, in spleen lymphocytes treated with DSS; however, such an increase was not observed in infected mice treated with DSS. Of particular interest, production of regulatory cytokines, IL-10 and transforming growth factor (TGF)-${\beta}$, in spleen lymphocytes showed a significant increase in mice infected with T. spiralis. A similar result was observed in mesenteric lymph nodes (MLN). Subsets of the population of $T_{reg}$ cells in MLN and spleen showed significant increases in mice infected with T. spiralis. In conclusion, T. spiralis infection can inhibit the DSS-induced colitis in mice by enhancing the regulatory cytokine and $T_{reg}$ cells recruitment.

• The Journal of Korean Obstetrics and Gynecology
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• v.18 no.4
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• pp.36-53
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• 2005

Purpose : The Purpose of this research was to investigate the effects of Haingkyunghonghwatang (HKHHT) on anti-inflammatory effects. Methods : As for the parameters of inflammation, levels of several inflammatory cytokines and chemical mediators were determined in mouse lung fibroblast cells(mLFC) and RAW264.7 cells. Also, changes in pathological features by drug treatment were investigated in the in vivo edema-induced rats by carrageenin/arachidonic acid or in the colitis-induced mice by DSS treatment. Results : The cytotoxicity of HKHHT on mLFC and RAW264.7 cells wasn't observed at 100, 50, 10, and $1{\mu}g/ml$ of The treatments. $IL-1{\beta}$, IL-6 and NOS-II mRNA expression of RAW264.7 cells was inhibited by The treatments in a dose-dependent manner. HKHHT treatment of RAW264.7cells(HtRc) inhibited $TNF-{\alpha}$ and COX-2 mRNA expression. HtRc significantly inhibited IL-6 and NO production. HtRc inhibited ROS production. HKHHT inhibited rat's paw edema induced by carrageenin or arachidonate treatment in all concentrations examined. The body weight and colon length of colitis-induced mice were recovered to a normal level by DSS treatment. Clinical disease levels were significantly improved compared to the control animals. HKHHT treatment of colitis-induced mice(HtCm) significantly increased hematological values such as WBC and RBC counts, Hgb and HCT levels, but decreased PLT values. HtCm decreased IL-6 and $TNF-{\alpha}$ production significantly HtCm significantly increased CD3+(T) cell counts. In contrast, HKHHT treatment decreased CD19+ B cell counts and CD3+/CD69+ significantly, and also decreased B/T ratio (%) though not significant. Conclusion : These results indicated that HKHHT could be used for treating diverse female diseases caused by the inflammation.

• The Journal of Korean Obstetrics and Gynecology
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• v.18 no.3
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• pp.92-109
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• 2005

Purpose : The Purpose of this research was to investigate the effects of Cheongyeolhawlhyeoltanggagyehyeoldeung (CYHHT) on anti-inflammatory effects. Methods : As for the parameters of inflammation, levels of several inflammatory cytokines and chemical mediators were determined in mouse lung fibroblast cells(mLFC) and RAW264.7 cells. Also, changes in pathological features by drug treatment were investigated in the in vivo edema-induced rats by carrageenin /arachidonic acid or in the colitis-induced mice by DSS treatment. Results : The cytotoxicity of CYHHT on mLFC and RAW264.7 cells was not observed at 100, 50, 10, and $1{\mu}g/ml$ of CYHHT treatments. $IL-1{\beta}$, IL-6 and NOS-IImRNA expression of RAW264.7 cells was inhibited by CYHHT treatments in a dose-dependent manner. CYHHT treatment of RAW264.7 cells inhibited $TNF-{\alpha}$ and COX-2 mRNA expression. CYHHT treatment of RAW264.7 cells significantly inhibited IL-6 and NO production. CYHHT treatment of RAW264.7 cells inhibited ROS production. CYHHT inhibited rat's paw edema induced by carrageenin or arachidonate treatment in all concentrations examined. The body weight and colon length of colitis-induced mice were recovered to a normal level by DSS treatment. Clinical disease levels were significantly improved compared to the control animals. CYHHT treatment of colitis-induced mice significantly increased hematological values such as WBC and RBC counts, Hgb and HCT levels, but decreased PLT values. CYHHT treatment of colitis-induced mice decreased IL-6 and $TNF-{\alpha}$ production significantly CYHHT treatment of colitis-induced mice significantly increased CD3+(T) cell counts. In contrast, CYHHT treatment decreased CD19+ B cell counts and CD3+/CD69+ significantly, and also decreased B/T ratio (%) though not significant. Conclusion : These results indicated that CYHHT could be used for treating diverse female diseases caused by the inflammation.

• Parasites, Hosts and Diseases
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• v.49 no.3
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• pp.245-254
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• 2011

Many immune down-regulatory molecules have been isolated from parasites, including cystatin (cystain protease inhibitor). In a previous study, we isolated and characterized Type I cystatin (CsStefin-1) of the liver fluke, Clonorchis sinensis. To investigate whether the CsStefin-1 might be a new host immune modulator, we induced intestinal inflammation in mice by dextran sodium sulfate (DSS) and treated them with recombinant CsStefin-1 (rCsStefin-1). The disease activity index (DAI) increased in DSS only-treated mice. In contrast, the DAI value was significantly reduced in rCsStefin-1-treated mice than DSS only-treated mice. In addition, the colon length of DSS only-treated mice was shorter than that of rCsStefin-1 treated mice. The secretion levels of IFN-${\gamma}$ and TNF-${\alpha}$ in the spleen and mesenteric lymph nodes (MLNs) were significantly increased by DSS treatment, but the level of TNF-${\alpha}$ in MLNs was significantly decreased by rCsStefin-1 treatment. IL-10 production in both spleen and MLNs was significantly increased, and IL-$10^+F4/80^+$ macrophage cells were significantly increased in the spleen and MLNs of rCsStefin-1 treated mice after DSS treatment. In conclusion, rCsStefin-1 could reduce the intestinal inflammation occurring after DSS treatment, these effects might be related with recruitment of IL-10 secreting macrophages.

• Journal of Cancer Prevention
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• v.21 no.2
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• pp.95-103
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• 2016

Background: Excess energy supply induces chronic low-grade inflammation in association with oxidative stress in various tissues including intestinal epithelium. The objective of this study was to investigate the effect of high-fat diet (HFD) on intestinal cell membrane integrity and intestinal tumorigenesis in $Apc^{Min/+}$ mice. Methods: Mice were fed with either normal diet (ND) or HFD for 12 weeks. The number of intestinal tumors were counted and biomarkers of endotoxemia, oxidative stress, and inflammation were determined. Changes in intestinal integrity was measured by fluorescein isothiocyanate (FITC)-dextran penetration and membrane gap junction protein expression. Results: HFD group had significantly higher number of tumors compared to ND group (P < 0.05). Blood total antioxidant capacity was lower in HFD group, while colonic 8-hydroxy-2'-deoxyguanosine level, a marker of oxidative damage, was higher in HFD group compared to that of ND group (P < 0.05). The penetration of FITC-dextran was substantially increased in HFD group (P < 0.05) while the expressions of membrane gap junction proteins including zonula occludens-1, claudin-1, and occludin were lower in HFD group (P < 0.05) compared to those in ND group. Serum concentration of lipopolysaccharide (LPS) receptor (CD14) and colonic toll-like receptor 4 (a LPS receptor) mRNA expression were significantly higher in HFD group than in ND group (P < 0.05), suggesting that significant endotoxemia may occur in HFD group due to the increased membrane permeability. Serum interleukin-6 concentration and myeloperoxidase activity were also higher in HFD group compared to those of ND group (P < 0.05). Conclusions: HFD increases oxidative stress disrupting intestinal gap junction proteins, thereby accelerating membrane permeability endotoxemia, inflammation, and intestinal tumorigenesis.