OBJECTIVE: To study the effects of interleukin-1β (IL-1β) on transdifferentiation of human embryonic lung fibroblasts to myofibroblasts and the effects of lentinan on the transdifferentiation. METHODS: The human embryonic lung fibroblasts were cultured in vitro, and fibroblasts were treated with different concentrations of IL-1β and lentinan. The proliferation activity of the human embryonic lung fibroblasts was evaluated by the Cell Counting Kit-8 (CCK-8). The expression of α-smooth muscle actin (α-SMA) protein was measured by immunocytochemistry. The levels of fibronectin (FN), typeⅠcollagen (ColⅠ) and α-SMA mRNA were detected by RT-PCR. RESULTS: Compared with the untreated control group, the absorbance value of cell proliferation, α-SMA protein levels, FN, ColⅠand α-SMA mRNA expression were significantly up-regulated after different concentrations of IL-1β (0.1, 1, 10 ng/mL) treatment for 48 hrs (P<0.01). Lentinan treatment inhibited up-regulation of the cell proliferation activity, α-SMA protein levels, FN, ColⅠand α-SMA mRNA expression induced by IL-1β in a dose-independent manner (P<0.01). CONCLUSIONS: Lentinan can suppress human embryonic lung fibroblast proliferation, fibroblast-myofibroblast transdifferentiation and extra cellular matrix synthesis induced by IL-1β.
Key words
Lentinan /
IL-1β /
α-smooth muscle actin /
Extra cellular matrix /
Human embryonic lung fibroblast
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References
［1］Davies DE. The role of epithelium in airway remodeling in asthma［J］. Proc Am Thorac Soc, 2009, 6(8): 678-682.
［2］Holgate ST, Arshad HS, Roberts GC, Howarth PH, Thurner P, Davies DE. A new look at the pathogenesis of asthma［J］. Clin Sci (Lond), 2009, 118(7):439-450.
［3］Rop O, Mlcek J, Jurikova T. Beta-glucans in higher fungi and their health effects［J］. Nutr Rev, 2009, 67(11):624-631.
［4］王蕾, 曹高忠, 叶乐平, 方丽. 香菇多糖对哮喘大鼠模型气管炎症反应及辅助性T淋巴细胞1/辅助性淋巴细胞2免疫应答失衡的调节［J］. 实用儿科临床杂志,2007,22(21):1630-1631.
［5］Tang ML, Wilson JW, Stewart AG, Royce SG. Airway remodell in asthma:current understanding and implications for future therapies［J］. Pharmacol Ther, 2006, 112(2):474-488.
［6］Bergeron C, Oulet LP. Structural changes in airway diseases characteristics, echanisms, onsequences, and pharmacologic modulation［J］. Chest, 129(4):1068-1087.
［7］Holgate ST, Davies DE, Lackie PM, Wilson SJ, Puddicombe SM, Lordan JL. Epithelial-mesenchymal interactions in the pathogenesis of asthma［J］. J Allergy Clin Immunol, 2000, 105(2 pt 1): 193-204.
［8］Knight DA, Lane CL, Stick SM. Does aberrant activation of the epithelial-mesenchymal trophic unit play a key role in asthma or is it an unimportant sideshow?［J］. Curr Opin Pharmacol, 2004, 4(3): 251-256.
［9］Holgate ST, Holloway J, Wilson S, Howarth PH, Haitchi HM, Babu S, et al. Understanding the pathophysiology of severe asthma to generate new therapeutic opportunities［J］. J Allergy Clin Immunol, 2006, 117(3): 496-506.
［10］Dinarello CA. Proinflammatory cytokines［J］. Chest, 2000, 188(2): 503-508.
［11］Lappalainen U, Whitsett JA, Wert SE, Tichelaar JW, Bry K. Interleukin-1beta causes pulmonary inflammation, emphysema, and airway remodeling in the adult murine lung［J］. Am J Respir Cell Mol Biol, 2005, 32(4):311-318.
［12］林立，李昌崇，管小俊，王晓丽，王强，张维溪，等.哮喘气道重塑大鼠肺组织磷酸化JNK、血清/BALF白介素1β表达变化［J］. 中国免疫学杂志, 2008, 24(10):952-955.
［13］Phan SH. Biology of fibroblasts and myofibroblasts［J］. Proc Am Thorac Soc, 2008, 5(3): 334-337.
［14］苏苗赏，李昌崇.纤维链接蛋白与支气管哮喘气道重构［J］. 国外医学:呼吸杂志分册, 2005, 25(9):682-684.
［15］Kirmaz C, Bayrak P, Yilmaz O, Yuksel H. Effects of glucan treatment on the Th1/Th2 balance in patients with allergic rhinitis a double-blind placebo-controlled study［J］. Eur Cytokine Netw, 2005, 16(2): 128-134.
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