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Effect of Smoking on the Expressional Levels of Matrix Metalloproteinase-9 and Its Inhabitor-1 in Sensitized Rats
Author: WangRuiYing
Tutor: DuYongCheng
School: Shanxi Medical
Course: Department of Respiratory Medicine
Keywords: Asthma Matrix metalloproteinase Tissue inhibitor of metalloproteinase Smoke
CLC: R562.25
Type: Master's thesis
Year: 2008
Downloads: 41
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Abstract
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Objective: To observe the smoking sensitized rat lung tissue matrix factor matrix metalloproteinase-9 and metalloproteinase tissue inhibitor 1 expression, and to explore the role of smoking in airway remodeling in asthma. : 24 clean male Wistar rats by random number table will be divided into a control group, sensitized group and smoking sensitized group, n = 8. The two groups after application of ovalbumin (OVA) sensitization and inhalation challenge, rat asthma model; inspire three weeks will be 30 minutes each time atomization smoking sensitized rats placed homemade smoked inside passive smoking, once a day, every 10 cigarettes, each burning cigarette 1 hour, 6 days a week, smoking a total of eight weeks. Detected by immunohistochemical method rat airway epithelial cell matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase 1 (TIMP-1) protein, the simultaneous measurement of the thickness of the bronchial wall; reverse transcription - polymerase MMP-9mRNA, TIMP-1mRNA chain reaction (RT-PCR) to detect the lung tissue content. Results: 1. Smoking sensitized group airway wall thickness (23.28 ± 2.38) was significantly higher than the sensitized group (20.06 ± 2.94) and control group (11.64 ± 2.43), the difference was statistically significant (P lt; 0.05); sensitized group higher, the difference was statistically significant (P lt; 0.05). 2 smoking sensitized group lung tissue expression of MMP-9mRNA airway epithelial cells in MMP-9 protein content (32.78 ± 2.60) (0.49 ± 0.02) was significantly higher than the sensitized group (0.41 ± 0.04; 23.05 ± 2.11) and control group (0.23 ± 0.03; 15.88 ± 1.69), the difference was statistically significant (P lt; 0.01); the sensitized group higher than that in the control group, the difference was statistically significant (P lt; 0.01). Smoking sensitized group lung tissue expression of TIMP-1mRNA airway epithelial cells in TIMP-1 protein content (34.54 ± 2.9) were higher than the sensitized group (0.37 ± 0.05 (0.53 ± 0.02); 21.25 ± 2.28) and control group (0.23 ± 0.04; 15.78 ± 1.97), the difference was statistically significant (P lt; 0.01); the sensitized group higher than that in the control group, the difference was statistically significant (P lt; 0.01). . Lung tissue MMP-9/TIMP-1mRNA ratio: smoking sensitized group (0.91 ± 0.05) is lower than the sensitized group (1.12 ± 0.06) and control group (1.03 ± 0.09), the difference was statistically significant (P lt ; 0.01); the sensitized group higher than that in the control group, the difference was statistically significant (P lt; 0.01). Airway epithelial cells MMP-9/TIMP-1 protein content ratio: Smoking sensitized group (0.94 ± 0.03) lower than the sensitized group (1.09 ± 0.07) and control group (1.01 ± 0.06), the difference was statistically significant respectively (P lt; 0.05, lt; 0.01); the sensitized group higher than that in the control group, the difference was statistically significant (P lt; 0.01). Conclusion: Smoking sensitized rat lung tissue can be MMP-9 and TIMP-1 overexpression, imbalance and increased airway remodeling.
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CLC: > Medicine, health > Internal Medicine > Respiratory system and chest diseases > Trachea and bronchial disease > Bronchial disease > Bronchial asthma
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