| ObjectiveGallstone is a global common disease, incident rate of which is about 10%. It is very harmful to peoples' health. In recent years, the ratio of gallstone (especially cholesterol gallstone) has been rising because of the developing of society and the advancing of people's standard of living. How to prevent and treat cholelithasis has been a concerning problem nowadays. The pathogenesis of cholelithasis has not been clarified yet, which including multi-factors. Besides the common factors such as cholesterol superaturation, biliary protein, biliary salt enterohepatic circulation and gallbladder motility, chronic inflammatory may also been concerned about.Now it is considered that the formation of cholesterol gallstone must include follow conditions: decompensation of liver, secreting supersaturation hepatobile, broken balance of nucleating proteins with anti-nucleating proteins, and declining of gallbladder motility, which for bile to have enough time to form concretions in the gallbladder. Many literatures have reported that immunoglobulins IgA, IgG, IgM are nucleating proteins in the bile. The primary origin of immunoglobulins in bile is the immunoglobulins in blood. It is found that IgA, IgG, IgM all have nucleating activity, especially IgG. IgG not only shortens the nucleating time, but also increases the amount and speed of crystalloid formation. Mucin is the primary component that mucus gallbladder epidermal cells excreted, and has been proved to be a nucleatingprotein by many scholars. But the pathogenesis of mucin's nucleation has not been clarified. Mucin is coded by MUC. Patients with cholesterol gallstones express specific MUC in the gallbladder epidermal cells.Cyclooxygenase (COX) or prostaglandin endoperoxide synthase (PGHs) is required for the conversion of arachidonic acid to prostaglandins, catalyzes the first step of the synthesis of prostanoids. COX is affinity with damnification and inflammation of alimentary canal mucosa , also with occurring and developing of digestive cancer. Two isoforms of this enzyme have been identified which are referred to as COX-1 and COX-2. COX-1 is constitutively expressed as a "housekeeping" enzyme in most tissues such as endothelial and smooth muscle. By contrast, COX-2 can be induced by various several physiological stimuli and pro-inflammatory agents, including lipopolysaccharide (LPS), cytokines, and growth factors. And it is up-regulated at sites of inflammation.Several studies have demonstrated that specific inhibitor of cyclooxygenase type 2 (COX-2) inhibits prostaglandin synthesis much like conventional NSAIDs. It can have anti-inflammatory and antialgesic activities without affecting prostaglandin synthesis at sites where classical NSAIDs have known toxicity. NSAIDs can reduce the risk of cholesterol gallstone formation by inhibition of COX-2-derived prostanoids facilitates the anti-inflammatory, analgesic, and antipyretic effects. However, many of the side effects of NSAIDs (e.g., gastrointestinal ulceration and bleeding, platelet dysfunctions) that caused by a suppression of COX-1 activity occurs. It suggested that specific COX-2 blocker may offer an alternative to traditional NSAIDs with fewer side effects. Certain study showed that specific COX-2 inhibitor is involved in the inflammatory response during chronic cholecystitis. Specific blockage of COX-2 reduced the PGE2 release to the inflamed gallbladder lumen. Whether specific COX-2 inhibitor could reduce the risk of cholesterol gallstone formation by affect inflammatory and it's functional mechanism raised our interest.The present study aimed to demonstrated the specific COX-2 inhibiter on gallbladder during lithogenic process by comparing the concentration ofimrmmoglobulins and raucin in bile and blood as well as the change of gallbladder and bile after using specific COX-2 inhibitor . We used rabbit models which were induced by high cholesterol diet (HCD) and certain group of which was interfered by specific COX-2 inhibitor celecoxib.MethodA total of 24 rabbits...
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