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Studying The Effect Of Yufeiyin Oand Its Decomposed Recipe On The Expression Of Smad2/3in Rats Which Have Pulmonary Fibrosis Developed From Acute Lung Injury

Posted on:2015-02-13Degree:MasterType:Thesis
Country:ChinaCandidate:Q LiangFull Text:PDF
GTID:2254330428470495Subject:Diagnostics of Chinese Medicine
Abstract/Summary:PDF Full Text Request
Objective:Based on the clinical and experimental studies on pulmonaryfibrosis developed from acute lung injury, combing the lung’s physiologicalproperty of “lung-qi governing falling and lung body favor moist”, to putforward the idea” lung Qi and Yin deficiency as the disease’s root and bloodstasis as the disease’s symptoms’. Through observing the rat model with thedisease that having been fed Yufeiyin and its decomposed recipes andcombing the theory “using the medicine to test the disease”, to reveal andperfect the changes of the pathogenesis of pulmonary fibrosis developed fromacute lung injury, to provide suggestions for setting standards for syndromeclassification in TCM, for accurate and quantifiable Curative effect assessmentsystem and for the standards to choose the medicine to assess the effectsobjectively.Method:The IPF SD Rat Model is established by using the trachealinstillation of BLM-A5to induce ALI.108rats are grouped randomly intocontrol group(below referred as Group A), model group(below referred asGroup B), buqitongluo group(below referred as Group C), yangyingtongluogroup(below referred as Group D), quyutongluo group (below referred asGroup E), and Yufeiyin group(below referred as Group F).Administeringnormal saline10ml/kg to Group A and Group B, buqitongluo suspension5.2g/kg to Group C, yangyintongluo suspension5.1g/kg to Group D,quyutongluo suspension5.3g/kg to Group E, Yufeiyin suspension12.4g/kgto Group F. Each group is administered intragastrically every day. To ensurethe model is successful, observe the rats’ weight, dieting, spirit, react,appearance, feces and so on. On the7th, the14th, and the28thexperiment day,catch6rats randomly from each group to anesthetize them, take blood fromfemoral artery, fix their right lower lung tissues in10%formaldehyde and then are made into paraffin microtomy. At last do HE dyeing, Masson dyeing, andimmunohistochemistry dyeing, freeze the remaining interstitial fluid withliquid nitrogen and preserved at-70℃for use, and then do the Western-blot.Result:(1) HE dyeing result show: Group A has clear pulmonaryorganizational structure, bright alveolar space. Alveolar wall didn’t becomethick; the structures of the alveolar epithelial cells were complete; pulmonaryinterstitium did’t have collagen deposition. As time goes by, Group B’spulmonary alveolitis and alveolar fibrosis became severe. On the7th day,some pulmonary alveoli and blood capillary became narrow and even closedwhich led to the substantive change of the lung tissue. There were a largenumber of activated macrophages; neutrophile granulocyte and lymphocyteare rarely seen; a large number of macrophages and inflammatory infiltrationappeared in the pulmonary interstitium. On the14th day, pulmonary alveolitiscontinued and inflammatory infiltration became obvious; some alveolidisappeared; the number of fibrocyte increased and pulmonary interstitialfibrosis showed, slight collagen began to deposit. On the28th day, alveolishrank; pulmonary interstitial fibrosis increased enormously; fibrous tissueoccupied the whole alveolar septum; some pulmonary alveoli streaked andtheir cicatrix changed; and scattered like chips.(2) Masson dyeing result show:Group A had slight blue Collagen fibers deposition around the trachea andblood vessel. On the7th day, there were fibroblast in the alveolar septum andmesenchyme, most of which concentrated on blood vessel, small and tinybronchus; slight blue Collagen fibers deposition appeared. On the14th day,the alveolar septum widened obviously; Collagen fibers deposition in the vasapublica, airway wall, alveolar septum, Interstitial increased enormously. Onthe28th day, flaky and streaky collagen fiber began to deposit in thepulmonary interstitium; pulmonary alveolus blended and changedfundamentally; the normal pulmonary fibrosis changed.(3)Immunohistochemistry dyeing and Western-blot show: Smad2/3and TGF-β inthe lung tissue kept expressing highly on the14th day and the28th day, and itreached the highest on the28th day.(4)After administering them, the rats from Group C, D, E, F, gradually changed progressively in pulmonary fibrosispathomorphology, but less than Group B; the expression trend of and Smad2/3and TGF-β1are similar to Group B, but the content is more than Group A, andless than Group B(P<0.05).Conclusion:1After the intervention of drugs, Smad2/3and TGF-β1are expressed inrats from Group C, Group D, Group E, Group F in a lower level than Group B,which indicates that the therapeutic effects of drugs to cure the disease isrelevant to the suppression of the expression of Smad2/3and TGF-β1.2The effect of dismantled recipes is not as good as the whole drug. Thetheory of “using the medicine to test the disease” indicates that thepathogenesis of the disease is Qi and Yin deficiency and obstruction of bloodnetwork vessel.
Keywords/Search Tags:Pulmonary Fibrosis, BLM-A5, TGF-β1, Signal Path, SD rat
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