Research On The Expression Of P38MAPK In Rat Achilles Tendon Enthesiopathy In Model

Research Purposes:Under normal physiological conditions, the mechanical factor plays an important regulatory role in cellular metabolism, growth, differentiation and matrix synthesis and degradation of bone and cartilage cells.Under the excessive or inappropriate stress stimulation, when bone and cartilage tissue can not produce a compensatory response, caused by the accumulation of the fine damage, exceeding the body’s ability to repair, leading related diseases. As an important medium for connecting cells and the external environment, p38 MAPK cell signaling pathway plays an important role in the transfer processes of stress stimulation from external to intracellular.Related diseases in the pathological process, the osteogenic differentiation of bone cells break, secretion of inflammatory factors, imbalances and cell apoptosis increased matrix synthesis and degradation processes such as are associated with increased expression of p38 MAPK. This essay focus on the changes of p38 MAPK in rats during Enthesiopathy under stress stimuli,trying to explain the mechanisms in theory.Research Methods:About 200 g of about 72 8-week-old male SD rats were purchased from the Experimental Animal Center of Soochow University,randomly divided into a control group and the experimental group(jumping group and burden jumping group),each group with 24 rats; within each category another group were randomly divided into 2 weeks, 4 weeks and 6 weeks groups of eight. Among them, the group using self-weight load jump 5% weight-bearing. Homemade electrical stimulation device modeling and the rats jump training for six weeks. In the second, fourth and sixth weeks after the test subjects, drawn parts, including Achilles, Achilles only at the point of cartilage and bone. HE staining process pathological changes observed terminal region of the organization, and immunohistochemical testing of its end zone p38 MAPK expression of tissue, measuring the number of cells positive for each site.Research Results:1. Enthesiopathy models successfulyl, according to HE staining results,having showed that the model group SD rats had terminal disease-related pathological changes, and modeling and post-weight-bearing rats have more significant pathological changes.2. No significant difference in the number of p38 MAPK positive cells in different parts of 2, 4, 6 weeks control group SD of rat Achilles tendon terminal area(P>0.05); 2 weeks jump group and weights jump group in all parts of the number of p38 MAPK positive cells increased, with statistical significance(P<0.05); 4 weeks jumpgroup of Achilles tendon and the weights jump group in all parts of the number of p38 MAPK positive cells was significantly increased, with statistical significance(P<0.05); 6 weeks jump group and weights jump group in all parts of the number of p38 MAPK positive cells was significantly increased, with statistical significance(P<0.05).3.No significant difference in the number of p-p38 MAPK positive cells in different parts of 2, 4, 6 weeks control group SD of rat Achilles tendon terminal area(P>0.05); 2 weeks jump group and weights jump group in all parts of the number of p-p38 MAPK positive cells was significantly increased, with significant difference(P<0.01); 4 weeks jump group the Achilles tendon and weights jump group in all parts of the number of p-p38 MAPK positive cells was significantly increased, with significant difference(P<0.01); 6 weeks jump group and weights jump group in all parts of thenumber of p-p38 MAPK positive cells was significantly increased, with significant difference(P<0.01).Research Conclusions:1. Under the effects of stress, rat terminal area gradually appear to have the terminal disease pathology.2.Stress can stimulate the expression of p38MAPK and p-p38MAPK to increase.激酶模式,反应包括4种激酶:PAK(p21 activated kinase,MAPKKKK)、MLK(MAPKKK、MKKK或MEKK)、MKK3/6/(MAPKK、MKK或MEK)、p38 MAPK...