“形寒饮冷则伤肺”的模拟研究与实质分析
摘要
目的:通过实验室模拟相应环境,对健康大鼠进行一定的刺激,以及对相关指标检测的评价,对中医经典理论“形寒饮冷则伤肺”的实质进行更深层次地探讨。
方法:选取健康Wistar雄性大鼠56只,随机分为以下4组:空白对照组、形寒组、饮冷组、形寒饮冷组,每组14只,将各组大鼠置于相应条件的调温箱或者给予相应的刺激,期间观察大鼠的一般情况变化及皮肤、毛发、饮食、便质、行为等变化,7日后采集标本,观测其肺组织病理改变,放免法检测血清CRP、肺组织匀浆IL-8的含量变化,酶免法检测β防御素在肺组织中的表达,原位杂交法检测TGFβ1-mRNA在肺组织及支气管上皮中的表达。应用SPSS13.0统计软件对实验数据进行统计学处理,并分析结果。
结果:形寒组、饮冷组、形寒饮冷组大鼠肺组织形态发生了明显改变,大鼠血清CRP升高,大鼠肺组织匀浆中IL-8含量升高、β防御素含量降低,以及TGFβ1-mRNA表达升高,其中形寒饮冷组最为显著,形寒组次之,饮冷组再次之。
结论:从多层次多角度进一步证实了“形寒”、“饮冷”与肺脏损伤之间存在的密切相关性,实验证明单纯“饮冷”亦可造成肺脏损伤,从一定程度上揭示了“形寒饮冷则伤肺”理论的内涵与实质,为拓展该理论的现代研究与应用范围提供了一定的思路、方法与依据。
AIM: To deep discuss Chinese Medicine classical theory“eating cold food in cold temperature will hurt the lung”through simulated atmosphere in the lab, and appraise concerned guidelines’inspection.
Method: Choose 56 healthy Wistar male rats, and divide them into 4 groups randomly, they are: control group, cold-temperature group, cold food-eating group, eating cold food in cold temperature group; 14 ones for each group. Put them into different temperature-controlled boxes or give them different stimulation. During this period, observe their changes, such as their skin, fur, food-eating, stool quality and behaviors. After 7 days, collect samples, observe their pathological changes in pulmonary tissue; exam serum CRP by radioimmunoassay method, the changes of pulmonary tissue homogenate IL-8 contents; examβalexin’s expression in pulmonary tissue through enzyme immunoassay; exam TGFβ1-mRNA’s expression in pulmonary tissue and bronchus through Situ Hybridization Method. Making statistical treating to the experimental data by applying SPSS13.0 statistics software, and analyze the results.
Result: The rats in cold-temperature group, cold food-eating group and eating cold food in cold temperature group, whose pulmonary tissues have obvious changes; i.e. serum CRP rose, IL-8 contents in rats’pulmonary tissue homogenate increased,βalexin contents decreased, and the expression of TGFβ1-mRNA increased; eating cold food in cold temperature group has most obvious symptom; cold-temperature group has less obvious symptom; the lest obvious symptom for cold food-eating group.
Conclusion: It’s proved further that“cold-temperature”and“cold food-eating”have close pertinence with lung hurt from multi-layer and multi-angle observation. The experiment also proved that single“cold food-eating”also can case lung hurt; it also reveals the connotation and essence of“eating cold food in cold temperature will hurt the lung”, so as to supply some ways or gist for developing the research and applied scope for this theory.
方法:选取健康Wistar雄性大鼠56只,随机分为以下4组:空白对照组、形寒组、饮冷组、形寒饮冷组,每组14只,将各组大鼠置于相应条件的调温箱或者给予相应的刺激,期间观察大鼠的一般情况变化及皮肤、毛发、饮食、便质、行为等变化,7日后采集标本,观测其肺组织病理改变,放免法检测血清CRP、肺组织匀浆IL-8的含量变化,酶免法检测β防御素在肺组织中的表达,原位杂交法检测TGFβ1-mRNA在肺组织及支气管上皮中的表达。应用SPSS13.0统计软件对实验数据进行统计学处理,并分析结果。
结果:形寒组、饮冷组、形寒饮冷组大鼠肺组织形态发生了明显改变,大鼠血清CRP升高,大鼠肺组织匀浆中IL-8含量升高、β防御素含量降低,以及TGFβ1-mRNA表达升高,其中形寒饮冷组最为显著,形寒组次之,饮冷组再次之。
结论:从多层次多角度进一步证实了“形寒”、“饮冷”与肺脏损伤之间存在的密切相关性,实验证明单纯“饮冷”亦可造成肺脏损伤,从一定程度上揭示了“形寒饮冷则伤肺”理论的内涵与实质,为拓展该理论的现代研究与应用范围提供了一定的思路、方法与依据。
AIM: To deep discuss Chinese Medicine classical theory“eating cold food in cold temperature will hurt the lung”through simulated atmosphere in the lab, and appraise concerned guidelines’inspection.
Method: Choose 56 healthy Wistar male rats, and divide them into 4 groups randomly, they are: control group, cold-temperature group, cold food-eating group, eating cold food in cold temperature group; 14 ones for each group. Put them into different temperature-controlled boxes or give them different stimulation. During this period, observe their changes, such as their skin, fur, food-eating, stool quality and behaviors. After 7 days, collect samples, observe their pathological changes in pulmonary tissue; exam serum CRP by radioimmunoassay method, the changes of pulmonary tissue homogenate IL-8 contents; examβalexin’s expression in pulmonary tissue through enzyme immunoassay; exam TGFβ1-mRNA’s expression in pulmonary tissue and bronchus through Situ Hybridization Method. Making statistical treating to the experimental data by applying SPSS13.0 statistics software, and analyze the results.
Result: The rats in cold-temperature group, cold food-eating group and eating cold food in cold temperature group, whose pulmonary tissues have obvious changes; i.e. serum CRP rose, IL-8 contents in rats’pulmonary tissue homogenate increased,βalexin contents decreased, and the expression of TGFβ1-mRNA increased; eating cold food in cold temperature group has most obvious symptom; cold-temperature group has less obvious symptom; the lest obvious symptom for cold food-eating group.
Conclusion: It’s proved further that“cold-temperature”and“cold food-eating”have close pertinence with lung hurt from multi-layer and multi-angle observation. The experiment also proved that single“cold food-eating”also can case lung hurt; it also reveals the connotation and essence of“eating cold food in cold temperature will hurt the lung”, so as to supply some ways or gist for developing the research and applied scope for this theory.
引文
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[4]徐艳玲.浅谈形寒寒饮伤肺咳[J].辽宁中医杂,2007;34(3):272-273.
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[4]徐艳玲.浅谈形寒寒饮伤肺咳[J].辽宁中医杂,2007;34(3):272-273.
[5]赵继红.从“聚于胃,关于肺”论咳嗽[J].浙江中医杂志,2002;(10):439-440.
[6]龙建新,姚广兴.关于“聚于胃,关于肺”的儿科临证体会[J].天津中医药, 2005;22(6):492.
[7]朱晋龙.也谈咳皆聚于胃关于肺[J].辽宁中医学院学报,2003;5(3):218-219.
[8]杨华.C-反应蛋白检测在呼吸系统疾病中的意义[J].临床军医杂志,2007; 35(1):115-117.
[9]陈晓红,程天民.C反应蛋白的药理学作用研究进展[J].中国药理学通报,1999;15(4):296-299.
[10]王前,郑磊,曾方银.超敏C反应蛋白的研究现状及临床应用[J].中华检验医学杂志,2004;27(8):542-544.
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[12] Larsen CG,Anderson AO,Appella E,et al.The neutro-phil-activating protein(NAP-1) is also chemo tactic for T lymphocytes[J].Science,1989;243(489):1464.
[13] Leonard EJ,Skeel A,Yoshimura T.etal.Leukocyte spe-cificity and binding of human neutrophil attractant/acti-vationprotein-1[J].Jour Immunology,1999;144(4):1323.
[14] Gerdt CR,etal.Bronchial inflammation in chronic bron-chitis assessed by measurement of cell products in bron-chial lavage fluid[J].Thorx,1995;50:360.
[15] Janice BY,etal. Interleukm 8:an important chemo at-tract antinspumm of patients with chronic inflammatory airway disease[J].Am J Physiol,1993;264:1413.
[16] Douglass JOh,etal.Influence of interleukm 8 challenge inthenasahnu eosaina topicand nontopxc subjects[J].Am J Respir Crit Care bled,1994;15(4):1108.
[17] Hass TH,Stitelman D,Davis SJ,etal.Egr-mediates extracellular matrix-driven transcription of membrane type 1 matrix metalloproteinase in endothelium[J]. J Biol hem,1999;27(32):22679-22685.
[18] David ACox,Thomasa Maurer .Cliimmuno and immuno pathology[M].1997;83:25.
[19] Dickson K, Philip A ,Warshsw ask H, etal.J Clin Invest[M].1995;95:2539.
[20] Hocevar-BA ,Howe-PH[J]. Miner-Electrolyte-Metab,1998;24:131.
[21] Stuart J Shankland ,Jeffrey Pipin, Raimunal H Pichler,etal. Kidney Int[M]. 1996, 50:116
[22] Zaninoni A,Imperiali FG, Pasquini C,etal. Cytokine modulation of nuclear factor-kappa B activity in B-chronic lymphocytic leukemia[J]. Exp Hematol, 2003; 31(3):185-190.
[23] Massague J .Cell[M],1996,85:947.
[24] Boer WI,van Schadewijk A,Sont JK,etal.Transforming growth factor beta 1 and recruitment of macrophages and mast cells in airways in chronic obstructive pulmonary disease[J].Am J Respir Crit Care Med,1998;158:1951-1957.
[25]韩玲,许建英.慢性阻塞性肺疾病患者气道上皮细胞TGF-β1表达的研究[J].山西医科大学学报,2007;38(7):31-33.
[26] Hazel JD,William MN,Kenneth DD,etal.Molecular mecha-nism of transforming growth factorβ1induced glutathione deplet-ing in alveolar epithelial cells[J].J Biol Chem,2002;277(24):21158-21166.
[27] Black PN,Young PG,Skinner SJ.Response of airway smooth muscle cells to TGF-beta1:effects on growth and synthesis of glycosaminoglycans[J]. Am J Physiol, 1996;271:910-917.
[28] Das SK,Fanburg BL.TGF-β1produces a“prooxidant”effect on bovine pulmonary artery endothelial cells in culture[J]. Am J Physiol,1991;261:249-254.
[29] White AC,Das SK,Fanburg BL. Reduction of glutathione is as-sociated with growth restriction and enlargement of bovine pul-monary artery endothelial cells produced by transforming growth factor-β1[J].Am J Respir Cell Mol Biol,1992;6:364-368.
[30] Kuschner WG,Alessandro A,Wang H,etal.Dose-dependent cigarette smoking- related inflammatory response in healthy adults [J]. Eur Respir J, 1996;9(10):1989-1994.
[31] Hazel JD,William MN,Kenneth DD,et al. Molecular mecha-nism of trans forming growth factorβ1induced glutathione deplet-ing in alveolar epithelial cells[J].J Biol Chem,2002;277(24):21158-21166.
[32]王伯瑶,吴琦.内源性抗生素肽-天然免疫的重要介质[J].生命科学,1991;11(增刊):64-66.
[33] Mak P,Wojcik K. Isolation.antimicrobial activities and primary structures of hamster neutrophil defensins[J]. Infect Immun,1996;64:4444.
[34]田翠环.β防御素与呼吸系统的防御和损伤[J].国外医学呼吸系统分册,2004;24(3):150-156.
[35] Jia HP,Wowk SA,Schutte BC,etal.A noval murine beta-defensin expressed in tongue,esophagus and trachea[J].J Biol Chem,2000;275:33314-33320.
[36]蔡绍晖,杜军,陈新年,等.克雷伯氏肺炎杆菌内毒素诱导小鼠β-防御素-4基因表达及其信号传递[J].华西医科大学学报,2001;32(2):157-162.
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