The Cold Evil Quantitative Simulation Study And The Related Factors Of The Lung

Objective:This study is based on clinical findings, laboratory simulation further relevantmeteorological factors, the impact of different levels of pathogenic cold and time todifferent stimuli in mice lungs and pulmonary system of pathogenic cold-induced diseasethrough analysis clinical observations, from pathology, cytokine gene expression andexplore the quantitative relationship between the angle of the relevant factors and pathogenic cold and pathogenic extent pulmonary disease, pulmonary disease deepen thequantitative theory of causative factors, and promoting medical quantification,standardization, scientific. Meanwhile, the issue of taking into account the evilrheumatism, by analyzing the effect of wind cold, dampness generated for cold diseases,thus providing some guidance and research for the prevention and treatment of respiratorydiseases.Methods: Before the start of the experiment all animals placed no wind, temperature (20±2)℃, humidity50%to55%of the environment adaptive feeding for1week, foodand water freely.First stage:Control group (N): The mice were placed in no wind, temperature (20±2)℃,humidity50%to55%of the rearing environment,4d after drawn.Experimental groups:T1Group: mice were placed in the refrigerator temperature, maintaining the temperature10℃, humidity50%~55%RH2hours stimulation.T2group: mice were placed in the refrigerator temperature, maintaining the temperature0℃, humidity50%~55%RH2hours stimulation.T3group: mice were placed in the refrigerator temperature, maintaining the temperature-10℃, humidity50%~55%RH2hours stimulation.T4group: mice were placed in the refrigerator temperature, maintaining the temperature0℃, humidity50%~55%RH stimulation4hours.T1group which stimulate completed immediately drawn, T2, T3, T4group drawn after4days of continuous stimulation.Second stage:Low group: mice were placed in the average wind speed3m/s, the temperature of0℃,humidity50%~55%RH2hours stimulation.Alpine Group: The mice were placed in no wind, temperature0℃,85%humidityenvironment to stimulate two hours. Cold Wind Group: The mice were placed in an average wind speed3m/s, temperature of0℃,85%humidity environment to stimulate two hours.Three groups of mice were stimulated four days of continuous coverage.Airway pathology observed under light microscope and make the appropriate pathologicalscore, ELISA assay in lung tissue TNF-α, changes in IL-1β, SOD, MDA content,HSP70mRNA expression levels were detected by RT-PCR in mice. Application SPSS18.0software for statistical analysis of experimental data, compared to the mice in each groupindex difference between the amount of pathogenic wind and explore the related factorsFanfei with lung lesions correlation.Results: The results from the statistics found in each experimental group of mice lungtissue homogenates TNF-α, IL-1β, SOD, MDA and HSP70mRNA levels werecompared with the control group appeared significantly higher (P <0.01). Compare thesame degree of pathogenic cold and exciting time two different experimental groups, thetemperature control at0℃, T4lung tissue of mice in TNF-α, IL-1β, SOD, MDA andHSP70mRNA content than T2group was increased (P <0.01); comparing the same timestimulate different levels of pathogenic cold experimental group of mice stimulated whentime is2hours, T3lung tissue of mice in TNF-α, IL-1β, SOD, MDA and HSP70mRNA content than the T2group was increased (P <0.01).Conclusion: Hanxie cause pathological changes in the lung and increased levels ofcytokines, and the extent of the increase with the growth of pathogenic cold and stimulusduration, the more severe lung damage. When Hanxie Fanfei shorter time being, cold evillittle effect on the degree of difference between lung injury. Pathogenic cold, windpathogenic cold, the wind cold dampness evil for varying degrees of damage to the lungs,and the pathogenic cold, cold evil to some extent, can significantly increase the damage tothe lungs to the body wind cold, wind cold dampness evil on the most serious damage tothe lungs.