| This thesis centers on the role of p38 Mitogen-activated protein kinase signaling pathways in inhibiting insulin resistance in myogenic IL-6. It investigates the changes of p38MAPK and the expression of IL-6 organizations and their function in improving or inhibiting the insulin resistance on rats with the intervention of sports and high-fat diet and the injection of carrier shRNA in muscle, liver, fat and blood.Objective The purpose of this thesis is to study the influence of myogenic IL-6 on insulin resistance toward high-fat dieted rats in aerobic stamina training and the intervention of shRNA and explores the action of p38MAPK in myogenic IL-6 to inhibit insulin resistance which aims at providing theoretical basis for understanding the mechanism of sports in improvingⅡdiabetes and searching for new treatment and target of metabolic syndrome.Methods First, 72 clean male SD rats of about 3 weeks old with the weight of 110士10g are selected. Then they are divided into 9 groups at random, which are Quiet, normal- fed group (A, n = 8), Quiet, high-fat fed group (B, n = 8), Exercise, high-fat fed group (C, n = 8), Exercise, high-fat fed shRNA group(D, n = 8), Exercise, high-fat fed, blank- carrier group (E, n = 8), Quiet, high-fat fed, shRNA group(F, n = 8), Quiet, high-fat fed, blank-carrier group (G, n = 8), Quiet, normal fed shRNA group (H, n = 8) and Quiet normal fed, blank-carrier group (I, n = 8). Third, the exercise group rats are trainied aerobicly for eight weeks, running once a day, six days a week. At the beginning, they run at a speed of 16m/min for 50min. A week later, the speed increases gradually by 1-m/min with the time prolonged to 5 minutes. In the eighth week, the rats run at a speed of 23m/min in the period of 85min. At the same time, they take the tail intravenous injection of shRNA carrier or blank carrierfor four times. The first tail intravenous injection begins on the day before formal aerobic training and the latter three take place on the free days after every two-week's exercises.Fourth, after eight weeks, all the rats are anesthetized to death. Their blood, muscle tissue (gastrocnemius and the soleus and quadriceps muscle), fat (abdominal fat) and hepatic are used to test the organization of protein expression p38MAPK through Western blot (protein imprinting) with glucose insulin sensitivity index through the positive sugar clamps technique, test IL-6 serum protein through ELISA, and the protein expression on organizations IL-6 through Real time-PCR. Then the relationship and causes related to the resistance index of insulin are analyzed, the changes of organizations IL–6 and p38MAPK protein between insulin resistance rat and exercise rat groups are compared and the causes are analyzed. At the end of the thesis, the influence of p38MAPK on myogenic IL-6 in inhibiting the insulin resistance is discussed on the basis of this experiment along with the previous research achievements.Conclusion (1) This study confirms that it is effective to establish insulin resistance model using high-fat diet method. (2) RNA is effective in interfering IL-6 gene expression and its organizations and blood is different from those of IL-6 express. (3) Different organizations of IL-6 and p38MAPK expression in rats have different texture characteristics and are influenced by movement. Sports leads to the rise of the liver, fat and muscle tissue IL - 6 in higher-fat- dieted rat, in which the rise in adipose tissue is the greatest; in high-fat-dieted rats, sports leads to the decrease of the expression quantity of p38MAPK in liver and fat, while it doesn't have a notable effect on the expression quantity in muscle tissue. (4) Aerobic stamina training can inhibit high-fat diets rats'insulin resistance from occurring, prevent and improve insulin resistance. (5) The increase of body movement and muscle-derived IL-6 express can improve or inhibit insulin resistance from happening. (6) IL-6 may improve or inhibit insulin resistance through p38MAPK signaling pathways, and there may be synergy between them; P38MAPK signaling pathways may play a key role when muscle-derived IL-6 is inhibiting insulin resistance. Further experiments are needed to confirm whether they are signal transduction factors of IL-6inhibit's insulin resistance. |
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