Researches On The Protection Mechanism Of Tea Polyphenols For Cigerrate Passive Smoking Injury Mice Lung

Smoking and passive smoking can cause serious harm to humanbeen.The passive smoking has particular significant for pregnant women, infants and young children,women and adolescents, it not only can cause a variety of respiratory diseases also cause lung injury and other lung diseases. Smokers face of numerous global phenomenon, smokers mitigate the harmful effects of smoking began increasingly dependent on tea, tea as an important health drinks, the key functional components of TeaPolyphe nols, Thealflavin and so has a strong antioxidant. Epidemiological studies found that polyphenols can interfere with the development of lung diseases, including lung cancer occurrence, and committed to the polyphenols as an anti-cancer drug development, and ultimately used in clinical trials, with the world of the "return to nature "the growing demand, the demand for natural medicines are also increasing, as one of the three tea beverages worldwide, the development of pharmacological functions will be greater efforts to promote tea drinking in the smoking population, play tea as a health effects of beverages.Such methods were used in our experiments. Smoke exposed mice was mode group, the remaining mice were randomly divided into three groups:Blank control group (C group10mice), low-tea polyphenols group (LTP group10mice) and high-tea polyphenols group (HTP group10mice). The group of LTP mice fed with polyphenols dose100mg/kg, the group of HTP mice fed with a dose of polyphenols200mg/kg. The mice were exposed in cigarette smoke for three consecutive months. Fumigation process was observed in mice with the quality of food intake and body weight of mice was measured survival.We took food and water after finished smoking, overnight, we got eyeball blood and put mice to death with cervical vertebra off. Take full of mice five lobes, camera, external visual observation of morphological changes of lung tissue, with10%formalin solution soak right upper lobe of mouse lung tissue for pathological analysis of lung tissue biopsy. Extracted the serum after of takeing mice eyeball and full blood. Detected the vigor of overall superoxide dismutase (T-SOD), glutathione peroxidase (GSH-PX), and the change of concentration for malondiald ehyde (MDA), interleuki n-6(IL-6), tumor necrosis factor-α (TNF-α) in mouse serum. Under the mouse lung tissue mRNA was extracted immediately first strand cDNA was synthesized in the housekeeping gene β-actin as an internal premise, using quantitative PCR method to study the differentially expressed for the pure smoke damage and deal with different concentrations of polyphenols smoke mouse lung tissue after injury interleukin6(IL-6), interleuki n-33(IL-33), tumor necrosis factor-α (TNF-α) and interleuki n-1β (IL-1β), etc. in total mRNA.The experimental results were obtain that:(1) Comparing with the control group the lungs were clear black and color dark heavy after exposed smoke and fed100mg/kg and200mg/kg dose TP on mice were improved markedly;(2) Comparing with normal control group, model group mice serum T-SOD, GSH-PX, MDA index were showing significant differences; Comparing with model group, LTP group mice serum T-SOD, GSH-PX, MDA index were showing significant differences; Comparing with normal control group, HTP group mice serum T-SOD, GSH-PX, MDA index were showing significant differences; Comparing with normal control group, passive model mice serum IL-6and TNF-α index were showing significant differences; Comparing with passive model group, LTP group mice serum IL-6and TNF-α index were showing significant differences; Comparing with passive model group, GTP group mice serum IL-6and TNF-α index were showing significant differences.(3) Comparing with the control group, in the cigarette smoke exposure in mice, the target gene IL-1β,IL-6, TNF-α, IL-33expression was significantly increased, reaching a significant difference. After fed with polyphenol, IL-1β, IL-6, TNF-α, IL-33expression had been increased to varying degrees, but comparing with the control group, HTP group had no difference in expression. After fed tea polyphenols whether mice lung morphology, serum oxidation index or inflammatory index had improved significantly, that tea polyphenols on the pulmonary damage caused by exposure to cigarette smoke had been certain repair effect. Previous experiments were simple discussion the establishment fumes model or relatively simple morphological, but in this experiment, the model discussed fumes after comparing mouse lung tissue morphology, and were differentially expressed mRNA total serum inflammatory factors in mice with vigor and determination of the content of a series of mouse lung tissue inflammatory markers, and had been more profound discussion at the molecular level. The experiment had a certain reference value in the prevention of lung disease.