• Title/Summary/Keyword: IL-22

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Effect of Codonopsis lanceolatae Extracts on Mouse IL-2, IFN-${\gamma}$, IL-10 Cytokine Production by Peritoneal Macrophage and the Ratio of IFN-${\gamma}$, IL-10 Cytokine (더덕 추출물의 경구 투여가 마우스의 사이토카인 생성과 IFN-${\gamma}$, IL-10 Ratio에 미치는 영향)

  • Ryu, Hye-Sook
    • The Korean Journal of Food And Nutrition
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    • v.22 no.1
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    • pp.69-74
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    • 2009
  • Codonopsis lanceolatae have been used as one of the traditional remedies as well as food source. We previously reported that in vitro supplementation of Codonopsis lanceolatae water extracts enhanced the splenocytes proliferation compared to the control group. This study, the combined immunomodulative effect of water extract Codonopsis lanceolatae was Seven to eight weeks old mice(balb/c) was fed ad libitum on chow diet and water extract of Codonopsis lanceolatae was orally administrated every other day for four weeks at two different concentrations(50 and 500 mg/kg B.W.). The production of cytokine(IL-2, IL-10 and IFN-${\gamma}$), secreted by macrophages stimulated with LPS or not, were detected by ELISA assay using the cytokine kit. The result of ex vivo study showed that the IL-2, IL-10 and IFN-${\gamma}$ was detected at 500 mg/kg B.W. supplementation group with LPS stimulation in all cases. Also, ratio of IFN-${\gamma}$, IL-10 was the range of 3${\sim}$7 with mitogen stimulation such as Con A and LPS. In conclusion, this study suggests that Codonopsis lanceolatae extracts may enhance the immune function by regulating the cytokine(IL-2, IL-10 and IFN-${\gamma}$) prodution capacity by activated macrophages in mice.

Morroniside on anti-inflammation activities in rats following acute myocardial infarction

  • Yu, Bangxing;Zhang, Guoxing;An, Yi;Wang, Wen
    • The Korean Journal of Physiology and Pharmacology
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    • v.22 no.1
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    • pp.17-21
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    • 2018
  • Our previous studies have confirmed that morroniside has neuroprotective effects. However, the effects of morroniside on cardiac myocardium remain unknown. Rats were anaesthetized with 10% chloral hydrate (0.35~0.4 mL/kg) and an acute myocardial infarction (AMI) was induced by ligating the anterior descending coronary artery (LAD). Following AMI, morroniside was administered intragastrically for 3 consecutive days at doses of 45, 90 and 180 mg/kg, respectively. Lactate dehydrogenase (LDH) and cardiac troponin T (cTnT) activities in AMI rats in the serum were detected with commercial kits. The expression of IL-6, $IL-1{\beta}$ and $TNF-{\alpha}$ in myocardium was detected by Western blotting analysis. We observed a significant decline in the Q(q) wave amplitude in morroniside-treated rats after 72 h. Additionally, treatment of morroniside decreased the levels of LDH and cTnT in AMI rats. We also observed that morroniside reduced the expression of IL-6, $IL-1{\beta}$ and $TNF-{\alpha}$ in myocardium. Taken together, our findings demonstrate that morroniside had effective anti-inflammatory properties in AMI rats.

Astaxanthin Ameliorates Atopic Dermatitis by Inhibiting the Expression of Signal Molecule NF-kB and Inflammatory Genes in Mice

  • Donghwan, Kim;Yong-Suk, Kim;Ho Sueb, Song
    • Journal of Acupuncture Research
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    • v.39 no.4
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    • pp.304-309
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    • 2022
  • Background: This study was conducted to determine the anti-inflammatory effect of astaxanthin, on atopic dermatitis. Methods: Changes in mouse body weight, lymph node weight, and the degree of improvement in symptoms were measured to determine the inflammatory response. Real-time reverse transcription-polymerase chain reaction tests were performed to determine the degree of expression of inflammation-related cytokines (IL-31 and IL-33 and chemokines such as CCL17 and CCL22), and western blot analysis was performed to evaluate the expression of inflammation-related factors (iNOS, COX-2, and NF-kB signaling molecules p-IkBα, p50, p-65 and pSTAT3). Results: The degree of symptoms significantly improved in the PA+AX group. Lymph node weight in the PA+AX group was lower than the PA group. Inflammatory cytokines (IL-31, IL-33, and inflammatory chemokines such as CCL17 and CCL22) were significantly reduced in the PA+AX group compared with the PA group. The expression of inflammatory genes (iNOS, COX-2, NF-kB and signaling molecules (p-IkBα, p50, p65, and p-STAT 3) was lower in the PA+AX group compared with the PA group. Conclusion: Astaxanthin may modulate the inflammatory response in a mouse model of atopic dermatitis and has an anti-inflammatory effect.

Targeting the Epithelium-Derived Innate Cytokines: From Bench to Bedside

  • Jongho Ham;Jae Woo Shin;Byeong Cheol Ko;Hye Young Kim
    • IMMUNE NETWORK
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    • v.22 no.1
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    • pp.11.1-11.26
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    • 2022
  • When epithelial cells are exposed to potentially threatening external stimuli such as allergens, bacteria, viruses, and helminths, they instantly produce "alarmin" cytokines, namely, IL-33, IL-25, and TSLP. These alarmins alert the immune system about these threats, thereby mobilizing host immune defense mechanisms. Specifically, the alarmins strongly stimulate type-2 immune cells, including eosinophils, mast cells, dendritic cells, type-2 helper T cells, and type-2 innate lymphoid cells. Given that the alarm-raising role of IL-33, IL-25, and TSLP was first detected in allergic and infectious diseases, most studies on alarmins focus on their role in these diseases. However, recent studies suggest that alarmins also have a broad range of effector functions in other pathological conditions, including psoriasis, multiple sclerosis, and cancer. Therefore, this review provides an update on the epithelium-derived cytokines in both allergic and non-allergic diseases. We also review the progress of clinical trials on biological agents that target the alarmins and discuss the therapeutic potential of these agents in non-allergic diseases.

Ethyl Acetate Fraction of Adenophora triphylla var. japonica Inhibits Migration of Lewis Lung Carcinoma Cells by Suppressing Macrophage Polarization toward an M2 Phenotype

  • Park, Shin-Hyung
    • Journal of Pharmacopuncture
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    • v.22 no.4
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    • pp.253-259
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    • 2019
  • Objectives: It is reported that tumor-associated macrophages (TAMs) contribute to cancer progression by promoting tumor growth and metastasis. The purpose of this study is to investigate the effect of different fractions of Adenophora triphylla var. japonica (AT) on the polarization of macrophages into the M2 phenotype, a major phenotype of TAMs. Methods: We isolated hexane, ethyl acetate, and butanol fractions from crude ethanol extract of AT. The cytotoxicity of AT in RAW264.7 cells was examined by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. RAW264.7 cells were polarized into the M2 phenotype by treatment with interleukin (IL)-4 and IL-13. The expression of M2 macrophage marker genes was detected by reverse transcription polymerase chain reaction (RT-PCR). The phosphorylation level of signal transducer and activator of transcription 6 (STAT6) was investigated by western blot analysis. The migration of Lewis lung carcinoma (LLC) cells was examined by transwell migration assay using conditioned media (CM) collected from RAW264.7 cells as a chemoattractant. Results: Among various fractions of AT, the ethyl acetate fraction of AT (EAT) showed the most significant suppressive effect on the mRNA expression of M2 macrophage markers, including arginase-1, interleukin (IL)-10 and mannose receptor C type 1 (MRC-1), up-regulated by treatment of IL-4 and IL-13. In addition, EAT suppressed the phosphorylation of STAT6, a critical regulator of IL-4 and IL-13-induced M2 macrophage polarization. Finally, the increased migration of Lewis lung carcinoma (LLC) cells by CM from M2-polarized RAW264.7 cells was reduced by CM from RAW264.7 cells co-treated with EAT and M2 polarization inducers. Conclusion: We demonstrated that EAT attenuated cancer cell migration through suppression of macrophage polarization toward the M2 phenotype. Additional preclinical or clinical researches are needed to evaluate its regulatory effects on macrophage polarization and anti-cancer activities.

Isoliquiritigenin attenuates spinal tuberculosis through inhibiting immune response in a New Zealand white rabbit model

  • Wang, Wenjing;Yang, Baozhi;Cui, Yong;Zhan, Ying
    • The Korean Journal of Physiology and Pharmacology
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    • v.22 no.4
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    • pp.369-377
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    • 2018
  • Spinal tuberculosis (ST) is the tuberculosis caused by Mycobacterium tuberculosis (Mtb) infections in spinal curds. Isoliquiritigenin (4,2',4'-trihydroxychalcone, ISL) is an anti-inflammatory flavonoid derived from licorice (Glycyrrhiza uralensis), a Chinese traditional medicine. In this study, we evaluated the potential of ISL in treating ST in New Zealand white rabbit models. In the model, rabbits (n=40) were infected with Mtb strain H37Rv or not in their $6^{th}$ lumbar vertebral bodies. Since the day of infection, rabbits were treated with 20 mg/kg and 100 mg/kg of ISL respectively. After 10 weeks of treatments, the adjacent vertebral bone tissues of rabbits were analyzed through Hematoxylin-Eosin staining. The relative expression of Monocyte chemoattractant protein-1 (MCP-1/CCL2), transcription factor ${\kappa}B$ ($NF-{\kappa}B$) p65 in lymphocytes were verified through reverse transcription quantitative real-time PCR (RT-qPCR), western blotting and enzyme-linked immunosorbent assays (ELISA). The serum level of interleukin (IL)-2, IL-4, IL-10 and interferon ${\gamma}$ ($IFN-{\gamma}$) were evaluated through ELISA. The effects of ISL on the phosphorylation of $I{\kappa}B{\alpha}$, $IKK{\alpha}/{\beta}$ and p65 in $NF-{\kappa}B$ signaling pathways were assessed through western blotting. In the results, ISL has been shown to effectively attenuate the granulation inside adjacent vertebral tissues. The relative level of MCP-1, p65 and IL-4 and IL-10 were retrieved. $NF-{\kappa}B$ signaling was inhibited, in which the phosphorylation of p65, $I{\kappa}B{\alpha}$ and $IKK{\alpha}/{\beta}$ were suppressed whereas the level of $I{\kappa}B{\alpha}$ were elevated. In conclusion, ISL might be an effective drug that inhibited the formation of granulomas through downregulating MCP-1, $NF-{\kappa}B$, IL-4 and IL-10 in treating ST.