Somatostatin In Mice With Hyperlipidemia Associated Acute Pancreatitis PI3K/PKB Cell Signaling Pathway

Objective: 1.To understand the changes of PI3K/PKB signal transduction pathway in hyperlipidemia acute pancreatitis, To further investigate the pathogenesis of hyperlipidemia acute pancreatitis。2. Study on the relationship between somatostatin and PI3K/PKB signal transduction, To understand the effect of somatostatin on PI3K/PKB cell signaling pathways, further clarify the mechanism of somatostatin in the treatment of hyperlipidemia acute pancreatitis. Methods: 1.the clean health male mice of kunming mice 30, 20~24g weight,Randomly divided into 3 groups, namely, the normal group(group A, n=10), hyperlipidemia sex pancreatitis group(group B, n=10), hyperlipidemia sex pancreatitis + somatostatin group(group C, n = 10). 2, group A: using ordinary food to feed.Group B and group C: using high fat diets(based feed ingredient 87.8% + 10% lard + 0. 2% cholesterol+2% cholic acid sodium). group A intraperitoneal injection of normal saline for control. Group B: the models of acute pancreatitis by intraperitoneal injection of caerulein plus lps. Group C: to establish animal model after subcutaneous injection of somatostatin for intervention. Three, 3 groups of mice after each of the 12 hours after the removal of the eye to take blood about 2ml, The blood lipids and serum amylase in serum samples were measured. ELISA method was used to detect the changes of serum cytokines(TNF-a, IL-1, etc). 4.take pancreatic tissue HE staining, observe the pathological changes of pancreas, Grewal standard is used for the pathological scoring and grading. Using immunohistochemical detection of PI3K/ PKB(phosphatidylinositol 3- kinase / protein kinase B) activity and expression of NF- kappa B(NF) expression.Collected data with mean ± standard difference(x±s) to describe the statistical data, analysis by using statistical software SPSS17.0, single factor variance analysis(one-way ANOVA) to compare the two groups of sample mean, P<0.05, that there were statistically significant differences. Results: 1.A, B, C three groups of mice by ordinary food and high-fat food after feeding, group B and group C mice than in group A dense hair shining, three groups of mice were compared to the initial weight, P<0.05,The difference was not statistically significant, group B, group C and group A final weight and the weight increment compared,P<0.05, the difference was statistically significant. 2.group B and group C, the serum TG(triglyceride), TC(total cholesterol) and Amy(amylase) higher than that in group A, use of somatostatin intervention, lower in group C than non intervention group B amylase, P<0.05, compared with statistical significance.3, using ELISA for detection of serum cell factor(TNF alpha, IL-1). Results show that: in group B and group C level was significantly higher than that of group A, the growth of endostatin endostatin intervention, group C level lower than group B, P<0.05, the differences were statistically significant. 4.group B and group C pancreatic tissue pathology score is higher than group A, P<0.05, which indicates that the AP model modeling success.At the same time, the C group was significantly higher than the A group, but lower than the B group, P<0.05, the difference was statistically significant. 5. The expression of PKB and NF- nuclear factor kappa B was detected by immunohistochemistry: group B and group C compared with the group A, the expression of two proteins increased, group B and group C of pancreatic tissue were higher than the IHS score of two proteins in the group A, P<0.05. the difference was statistically significant. IHS score of pancreatic tissue in group C was lower than that in group B, P<0.05. the difference was statistically significant, suggesting that somatostatin could down regulate the expression of two protein in pancreatic tissue of mice with hyperlipidemia and acute pancreatitis. Conclusion: 1.with hyperlipidemia acute pancreatitis,PI3K/PKB signal transduction pathway by up regulation of nuclear factor kappa B,TNF-a and cytokine alpha and IL-1 production,In order to promote the occurrence and development of pancreatic tissue inflammatory response in patients with hyperlipidemia acute pancreatitis. 2.with the occurrence and development of somatostatin inhibition of PI3K/PKB signal transduction pathway and down-regulation of NF- kappa B and cytokines TNF-α and IL- 1, thus reducing the role of-1 in acute pancreatitis.