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RISS 인기검색어
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- 저자 : Chian-Jiun Liou (검색결과 2 건)
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Chian-Jiun Liou,,Pei-Yun Cheng,Wen-Chung Huang,Cheng-Chi Chan,Meng-Chun Chen,Ming-Ling Kuo,Jiann-Jong Shen 대한천식알레르기학회 2014 Allergy, Asthma & Immunology Research Vol.6 No.6
Purpose: Lovastatin is an effective inhibitor of cholesterol synthesis. A previous study demonstrated that lovastatin can also suppress airway hyperresponsiveness (AHR) in murine model of asthma. We aimed to investigate the effect of lovastatin on mucus secretion and inflammation-associated gene expression in the lungs of murine model of asthma. Methods: Female BALB/c mice were sensitized and challenged with ovalbumin (OVA) by intraperitoneal injection, and orally administered lovastatin from days 14 to 27 post-injection. Gene expression in lung tissues was analyzed using real-time polymerase chain reaction. AHR and goblet cell hyperplasia were also examined. BEAS-2B human bronchial epithelial cells were used to evaluate the effect of lovastatin on the expression of cell adhesion molecules, chemokines, and proinflammatory cytokines in vitro. Results: We showed that lovastatin inhibits the expression of Th2-associated genes, including eotaxins and adhesion molecules, in the lungs of murine model of asthma. Mucin 5AC expression, eosinophil infiltration and goblet cell hyperplasia were significantly decreased in the lung tissue of murine model of asthma treated with lovastatin. Furthermore, lovastatin inhibited AHR and expression of Th2-associated cytokines in bronchoalveolar lavage fluid. However, a high dose (40 mg/kg) of lovastatin was required to decrease specific IgE to OVA levels in serum, and suppress the expression of Th2-associated cytokines in splenocytes. Activated BEAS-2B cells treated with lovastatin exhibited reduced IL-6, eotaxins (CCL11 and CCL24), and intercellular adhesion molecule-1 protein expression. Consistent with this, lovastatin also suppressed the ability of HL-60 cells to adhere to inflammatory BEAS-2B cells. Conclusions: These data suggest that lovastatin suppresses mucus secretion and airway inflammation by inhibiting the production of eotaxins and Th2 cytokines in murine model of asthma.
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Ginsenoside Rg3 ameliorates allergic airway infl ammation and oxidative stress in mice
Wen-Chung Huang,Tse-Hung Huang,Kuo-Wei Yeh,Ya-Ling Chen,Szu-Chuan Shen,Chian-Jiun Liou 고려인삼학회 2021 Journal of Ginseng Research Vol.45 No.6
Background: Ginsenoside Rg3, isolated from Panax ginseng, has anti-inflammatory and anti-tumor activities. It is known to reduce inflammation in acute lung injury in mice, and to reduce the expression ofinflammatory cytokines and COX-2 in human asthmatic airway epithelium. In this study, we attemptedto determine whether ginsenoside Rg3 inhibits airway inflammation, oxidative stress, and airwayhyperresponsiveness (AHR) in the lungs of asthmatic mice. We also investigated its effects on oxidativestress and the inflammatory response in tracheal epithelial cells. Methods: Asthma symptoms were induced in female BALB/c mice sensitized with ovalbumin (OVA). Micewere divided into five groups: normal controls, OVA-induced asthmatic controls, and asthmatic micetreated with ginsenoside Rg3 or prednisolone by intraperitoneal injection. Inflammatory BEAS-2B cells(human tracheal epithelial cells) treated with ginsenoside Rg3 to investigate its effects on inflammatorycytokines and oxidative responses. Results: Ginsenoside Rg3 treatment significantly reduced eosinophil infiltration, oxidative responses,airway inflammation, and AHR in the lungs of asthmatic mice. Ginsenoside Rg3 reduced Th2 cytokineand chemokine levels in bronchoalveolar lavage fluids and lung. Inflammatory BEAS-2B cells treated withginsenoside Rg3 reduced the eotaxin and pro-inflammatory cytokine expressions, and monocyteadherence to BEAS-2B cells was significantly reduced as a result of decreased ICAM-1 expression. Furthermore, ginsenoside Rg3 reduced the expression of reactive oxygen species in inflammatory BEAS-2B cells. Conclusion: Ginsenoside Rg3 is a potential immunomodulator that can ameliorate pathological featuresof asthma by decreasing oxidative stress and inflammation
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