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The purpose of acute pancreatitis (Acute Pancreatitis, AP) in the pathogenesis, cytokines and inflammation imbalance theory has been unanimously recognized by everyone, a number of cytokines produced in the AP mediates inflammatory mediators increase the sticky surface of endothelial cells with the expression of molecules, causing localized neutrophil adhesion, aggregation, activation of neutrophils produce cytokines and inflammatory mediators of local cytotoxic effects, and cause changes in vascular permeability, platelet aggregation, thrombosis, caused pancreatic microcirculation, increased pancreatic injury, so the vicious cycle of the pancreas and peripancreatic tissue self-digestion, local inflammatory cytokines produced by the reaction into the blood circulation, continues through the reaction of a large waterfall type cytokines, produce systemic effects, local inflammation of progression to systemic inflammatory response (SIRS). Leptin (Leptin) as an obesity gene encoding the protein product, with a variety of physiological functions in the body may be involved in a variety of metabolic regulation, a number of scholars have found many ways you can Leptin activation of immune cells, especially CD4 T cells, increased cell immune function, and through anti-inflammatory and pro-inflammatory cytokine expression reflected increased or decreased, while in the body, hunger and inflammatory infection, serum leptin levels were significantly increased, which speculated that it may in the host inflammatory reactions play an important protective role. Endogenous nitric oxide (NO) is L-arginine (L-Arg) as a substrate of nitric oxide synthase (NOS) mediated by coenzyme Ⅱ (NADPH) to provide electronic, yellow Su nucleotide (FMN), flavin adenine dinucleotide (FAN), tetrahydrobiopterin (BH4) and iron atoms (Fe) electron transfer, with a combination of molecular oxygen. NOS has been found in the structure of three types: endothelial (ecNOS) brain type (bcNOS), and brain endothelial cells were isolated from the two referred to the native enzyme (cNOS), mainly in endothelial cells, nerve cells, smooth muscle cells and platelets. Physiological circumstances there cNOS gene expression of endogenous vasoactive substances stimulate increased intracellular calcium concentration, activation of cNOS synthetic small NO, the main transmission medium and adjust the media to play a role. The third type is known as macrophage inducible enzyme (iNOS), mainly in macrophages, mast cells, neutrophils, fibroblasts, hepatocytes, pancreatic islet cells and gastrointestinal mucosa cells and other cells, Some cells with native enzymes, such as endothelial cells, smooth muscle cells and nerve cells, also have the enzyme present. INOS gene under physiological conditions is not expressed, and only some of endotoxin and cytokines such as TNF, γ-IFN, IL-1 and other stimuli can be transcribed and translated under the catalytic L-Arg generate a lot of NO, in vivo non-specific immunity Anti-tumor tissue and invading microorganisms, accompanied by the release of NO and superoxide anion generation, which together with N0 can cause oxidative tissue damage and necrosis. Leptin can stimulate the release of nitric oxide various tissues, NO effect on the AP has two sides, that both the protective effect of NO, there are cytotoxic and proinflammatory effects. Exactly what effect dominates depends on NO production location, number and duration of action. Play a protective role for NO mostly by calcium-dependent cN0S synthesis and release, and caused major damage to the role of NO and non-calcium-dependent iNOS relevant. This study investigated exogenous leptin (Leptin) in patients with acute pancreatitis (AP) in nitric oxide (NO), nitric oxide synthase (NOS) expression and its effect on pancreatic injury. Method 1. Determined using isotope labeling method cNOS and iNOS activity. (2) Determination of nitrate reductase pancreatic tissue NO 2 - / NO 3 - content. 3 pancreatic tissue morphology and microscopic examination of pancreatic tissue injury quantitative assessment. Results 1. Pancreatitis rat pancreatic tissue NO, iNOS content and pathological quantitative scores were significantly higher than the sham group, while cNOS activity was significantly decreased. 2 by pancreatitis Leptin treatment group compared with the display: Leptin treated rats pancreatic tissue cNOS activity increased, while iNOS activity was significantly decreased, NO concentration is decreased but still higher than the sham group, the pathological quantitative score significantly lower than the AP group. Conclusions The results suggest that acute pancreatitis, iNOS activity increased, while cNOS activity decreased, NO generation increased significantly. After giving Leptin, iNOS greatly reduced, but not with the content of NO and iNOS and greatly reduced, which may be given after Leptin it causes a corresponding increase in the result of cNOS, the pancreatic tissue injury is significantly reduced, so that, Leptin through: (a) reducing excessive iNOS catalyzed NO, mitigate their produce cytotoxicity. (2) to increase its catalytic cNOS generated NO, play a physiological endogenous NO and protection, improve pancreatic tissue microcirculation blood flow. Leptin through the above channels play its protective effect on the pancreas, thereby accelerating the recovery of acute pancreatitis, which proves Leptin in acute pancreatitis pancreatic tissue is one of the important protective factor for its clinical application provide a theoretical basis.
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