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School of Basic Medical Sciences, Beijing University of Chinese Medicine,Beijing,China
纸质出版日期:2015,
网络出版日期:2014-12-18,
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Wang, T., Zhong, Xg., Li, Yh. et al. Protective effect of emodin against airway inflammation in the ovalbumin-induced mouse model., Chin. J. Integr. Med. 21, 431–437 (2015). https://doi.org/10.1007/s11655-014-1898-z
Tan Wang, Xiang-gen Zhong, Yu-hang Li, et al. Protective effect of emodin against airway inflammation in the ovalbumin-induced mouse model[J]. Chinese Journal of Integrative Medicine, 2015,21(6):431-437.
Wang, T., Zhong, Xg., Li, Yh. et al. Protective effect of emodin against airway inflammation in the ovalbumin-induced mouse model., Chin. J. Integr. Med. 21, 431–437 (2015). https://doi.org/10.1007/s11655-014-1898-z DOI:
Tan Wang, Xiang-gen Zhong, Yu-hang Li, et al. Protective effect of emodin against airway inflammation in the ovalbumin-induced mouse model[J]. Chinese Journal of Integrative Medicine, 2015,21(6):431-437. DOI: 10.1007/s11655-014-1898-z.
To investigate whether emodin exerts protective effects on mouse with allergic asthma. A mouse model of allergic airway inflflammation was employed. The C57BL/6 mice sensitized and challenged with ovalbumin (OVA) were intraperitoneally administered 10 or 20 mg/kg emodin for 3 days during OVA challenge. Animals were sacrificed 48 h after the last challenge. Inflammatory cell count in the bronchoalveolar lavage fluid (BALF) was measured. The levels of interleukin (IL)-4
IL-5
IL-13 and eotaxin in BALF and level of immunoglobulin E (IgE) in serum were measured with enzyme-linked immuno sorbent assay kits. The mRNA expressions of IL-4
IL-5
heme oxygenase (HO)-1 and matrix metalloproteinase-9 (MMP-9) were determined by real-time quantitative polymerase chain reaction. Emodin induced significant suppression of the number of OVA-induced total inflammatory cells in BALF. Treatment with emodin led to significant decreases in the levels of IL-4
IL-5
IL-13 and eotaxin in BALF and total IgE level in serum. Histological examination of lung tissue revealed marked attenuation of allergen-induced lung eosinophilic inflammation. Additionally
emodin suppressed IL-4
IL-5 and MMP-9 mRNA expressions and induced HO-1 mRNA expression. Emodin exhibits anti-inflammatory activity in the airway inflammation mouse model
supporting its therapeutic potential for the treatment of allergic bronchial asthma.
To investigate whether emodin exerts protective effects on mouse with allergic asthma. A mouse model of allergic airway inflflammation was employed. The C57BL/6 mice sensitized and challenged with ovalbumin (OVA) were intraperitoneally administered 10 or 20 mg/kg emodin for 3 days during OVA challenge. Animals were sacrificed 48 h after the last challenge. Inflammatory cell count in the bronchoalveolar lavage fluid (BALF) was measured. The levels of interleukin (IL)-4
IL-5
IL-13 and eotaxin in BALF and level of immunoglobulin E (IgE) in serum were measured with enzyme-linked immuno sorbent assay kits. The mRNA expressions of IL-4
IL-5
heme oxygenase (HO)-1 and matrix metalloproteinase-9 (MMP-9) were determined by real-time quantitative polymerase chain reaction. Emodin induced significant suppression of the number of OVA-induced total inflammatory cells in BALF. Treatment with emodin led to significant decreases in the levels of IL-4
IL-5
IL-13 and eotaxin in BALF and total IgE level in serum. Histological examination of lung tissue revealed marked attenuation of allergen-induced lung eosinophilic inflammation. Additionally
emodin suppressed IL-4
IL-5 and MMP-9 mRNA expressions and induced HO-1 mRNA expression. Emodin exhibits anti-inflammatory activity in the airway inflammation mouse model
supporting its therapeutic potential for the treatment of allergic bronchial asthma.
AsthmaEmodinairway inflammationChinese Medicine
AsthmaEmodinairway inflammationChinese Medicine
Lee YS, Han OK, Park CW, Yang CH, Jeon TW, Yoo WK, et al. Pro-inflammatory cytokine gene expression and nitric oxide regulation of aqueous extracted Astragali radix in RAW 264.7 macrophage cells. J Ethnopharmacol 2005;100:289–294.
Elias JA, Lee CG, Zheng T, Ma B, Homer RJ, Zhu Z. New insights into the pathogenesis of asthma. J Clin Invest 2003;111:291–297.
Kay AB. Allergy and allergic diseases. First of two parts. N Engl J Med 2001;344:30–37.
Lu Y, Yang JH, Li X, Hwangbo K, Hwang K, Taketomi Y, et al. Emodin, a naturally occurring anthraquinone derivative, suppresses IgE-mediated anaphylactic reaction and mast cell activation. Biochem Pharmacol 2011;82:1700–1708.
Song ZC, Wang ZS, Bai JH, Li Z, Hu J. Emodin, a naturally occurring anthraquinone, ameliorates experimental autoimmune myocarditis in rats. Tohoku J Exp Med 2012;227:225–230.
Chen ZF, Zhang L, Yi JY, Yang ZB, Zhang ZJ, Li Z. Promotion of adiponectin multimerization by emodin: a novel AMPK activator with PPARβ-agonist activity. J Cell Biochem 2012;11:3547–3558.
Marino R, Theraisingam T, Camateros P, Kanagaratham C, Xu YZ, Henri J, et al. Secretory leukocyte protease inhibitor plays an important role in the regulation of allergic asthma in mice. J Immunol 2011;7:4433–4442.
Papi A, Caramori G, Adcock IM, Barnes PJ. Rescue treatment in asthma. More than as-needed bronchodilation. Chest 2009;135:1628–1633.
Barnes PJ, Adcock IM. Glucocorticoid resistance in inflammatory diseases. Lancet 2009;373:1905–1917.
Ohkawara Y, Lei XF, Stämpfli MR, Marshall JS, Xing Z, Jordana M. Cytokine and eosinophil responses in the lung, peripheral blood, and bone marrow compartments in a murine model of allergen-induced airways inflammation. Am J Respir Cell Mol Biol 1997;16:510–520.
Wegmann M, Fehrenbach H, Fehrenbach A, Held T, Schramm H, Garn H, et al. Involvement of distal airways in a chronic model of experimental asthma. Clin Exp Allergy 2005;35:1263–1271.
Yamaoka KA, Dugas B, Paul-Eugene N, Mencia-Huerta JM, Braquet P, Kolb JP. Leukotriene B4 enhances IL-4-induced IgE production from normal human lymphocytes. Cell Immunol 1994;156:124–134.
Robinson D, Hamid Q, Bentley A, Ying S, Kay AB, Durham SR. Activation of CD4+ T cells, increased TH2-type cytokine mRNA expression, and eosinophil recruitment in bronchoalveolar lavage after allergen inhalation challenge in patients with atopic asthma. J Allergy Clin Immunol 1993;92:313–324.
Palframan RT, Collins PD, Williams TJ, Rankin SM. Eotaxin induces a rapid release of eosinophils and their progenitors from the bone marrow. Blood 1998;91:2240–2248.
Choi AM, Alam J. Heme oxygenase-1: function, regulation, and implication of a novel stress-inducible protein in oxidantinduced lung injury. Am J Respir Cell Mol Biol 1996;15:9–19.
Barnes PJ. Reactive oxygen species and airway inflammation. Free Radic Biol Med 1990;9:235–243.
Kharitonov SA, Chung KF, Evans D, O’Connor BJ, Barnes PJ. Increased exhaled nitric oxide in asthma is mainly derived from the lower respiratory tract. Am J Respir Crit Care Med 1996;153:1773–1780.
Carter EP, Garat C, Imamura M. Continual emerging roles of HO-1: protection against airway inflammation. Am J Physiol Lung Cell Mol Physiol 2004;287:L24–L25.
Ryter SW, Alam J, Choi MK. Heme oxygenase-1/carbon monoxide: from basic science to therapeutic applications. Physiol Rev 2006;86:583–650.
Fredenburgh LE, Perrella MA, Mitsialis SA. The role of heme oxygenase-1 in pulmonary disease. Am J Respir Cell Mol Biol 2007;36:158–165.
Vogt BA, Alam J, Croatt AJ, Vercelloth GM, Nath KA. Acquired resistance to acute oxidative stress. Possible role of heme oxygenase and ferritin. Laborat Invest 1995;72:474–483.
Almolki A, Taille C, Martin GF, Jose PJ, Zedda C, Conti M, et al. Heme oxygenase attenuates allergen-induced airway inflammation and hyperreactivity in guinea pigs. Am J Physiol Lung Cell Mol Physiol 2004;287:L26–L34.
Keshavan P, Deem TL, Schwemberger SJ, Babcock GF, Cook-Mills JM, Zucker SD. Unconjugated bilirubin inhibits VCAM-1-mediated transendothelial leukocyte migration. J Immunol 2005;174:3709–3718.
Kelly EA, Busse WW, Jaejour NN. Increased matrix metalloproteinase-9 in the airway after allergen challenge. Am J Respir Crit Care Med 2000;162:1157–1161.
Mautino G, Oliver N, Chanez P, Bousquet J, Capony M. Increased release of matrix metalloproteinase-9 in bronchoalveolar lavage fluid and by alveolar macrophages of asthmatic. Am J Respir Cell Mol Biol 1997;17:583–591.
Pérez-Ramos J, de Lourdes Segura-Valdez M, Vanda B, Selman M, Pardo A. Matrix metalloproteinases 2, 9, and 13, and tissue inhibitors of metalloproteinases 1 and 2 in experimental lung silicosis. Am J Respir Crit Care Med 1999;160:1274–1282.
Tan RJ, Fattma CL, Niehouse LM, Tobolewski JM, Hanford LE, Li Q. Matrix metalloproteinases promoted inflammation and fibrosis in asbestosis-induced lung injury in mice. Am J Respir Cell Mol Biol 2006;35:289–297.
Okada S, Kita H, George TJ, Gleich GJ, Leiferman KM. Migration of eosinophils through basement membrane components in vitro: role of matrix metalloproteinase-9. Am J Respir Cell Mol Biol 1997;17:519–528.
Delclaux C, Delacourt C, D’Ortho MP, Boyer V, Lafuma C, Harf A. Role of gelatinase B and elastase in human polymorphonuclear neutrophil migration across basement membrane. Am J Respir Cell Mol Biol 1996;14:288–295.
Cataldo D, Munaut C, Noël A, Frankenne F, Bartsch P, Foidart JM, et al. MMP-2- and MMP-9-linked gelatinolytic activity in the sputum from patients with asthma and chronic obstructive pulmonary disease. Intern Archiv Allergy Immunol 2000;123:259–267.
Russell REK, Culpitt SV, DeMatos C, Donnelly L, Smith M, Wiggins J, et al. Release and activity of matrix metalloproteinase-9 and tissue inhibitor of metal oproteinase-1 by alveolar macrophages from patients with chronic obstructive pulmonary disease. Am J Respir Cell Mol Biol 2002;26:602–609.
Lanchou J, Corbel M, Tanguy M, Germain N, Boichot E, Theret N. Imbalance between matrix metalloproteinases (MMP-9 and MMP-2) and tissue inhibitors of metalloproteinases (TIMP-1 and TIMP-2) in acute respiratory distress syndrome patients. Critic Care Med 2003;31:536–542.
Lee YC, Song CH, Lee HB, Oh JL, Rhee YK, Park HS, et al. A murine model of toluene diisocyanate-induced asthma can be treated with matrix metalloproteinase inhibitor. J Allergy Clin Immunol 2001;108:1021–1026.
Lee KS, Jin SM, Kim HJ, Lee YC. Matrix metalloproteinase inhibitor regulates inflammatory cell migration by reducing ICAM-1 and VCAM-1 expression in a murine model of toluene diisocyanate-induced asthma. J Allergy Clin Immunol 2003;111:1278–1284.
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