| Cyclooxygenase(COX) is a rate-limiting enzyme which can catalyze biosynthesis of prostaglandin and turn arachidonic acid (AA) into prostaglandin G2(PGG2), H2(PGH2).After the conversion has happened, COX will automatically and quickly be inactivated; So, Cox is unceasingly re-synthesized to keep production of PG. Series of PG have extensive functions in vivo. Except attending some important physiologic reaction such as blood coagulation, ovulation, parturition, immune response sustained by renal function, PGs exert capital function in inflammatory reaction. 1. At present, Cox has been found two sub-types, COX-1 and COX-2. COX-1 is a structural gene of mammal, called housekeeping gene, and can take part in the reaction of gastric mucosa protection, regulation of renal blood flow, and control of platelet aggregation. On the contrary, COX-2 mRNA and corresponding protein can hardly be detected in normal tissue, but induced by inflammation and mitogen including cytokines, endotoxin and interleukin to take part in reactions of inflammation, cell proliferation and differentiation.2. Scientific- research- personnel in the west and Japan have carried out a great deal of researches on COX-2, especially about the relationship between COX-2 and tumor, and also found the relation between NSAIDs and tumor. They identically think that, it may be the function of COX-2 suppression to interpret decreased incidence rate and mortality rate of cancer of colon when using NSAIDs, but clear mechanism is unknown. According to advanced study, there are special function of COX-2 in inflammation, ache and tumor generation; It is probably an early sign of tumor generation that high expression of COX-2 mRNA and corresponding protein in tissue, and also may be the target in controlling inflammation, relieving aches, even preventing and curing cancer.[25] However, there are little reports on COX-2 expression and corresponding protein in tissue suffering pulpitis. This text analyzes the close correlation between COX-2 and inflammation occurrence and development through the study of expressions of COX-1 and COX-2 in dental pulp. We apply immunohistochemistry methods in this study to report expressions of COX-1 and COX-2 in dental pulp: COX-1 has been expressed in normal and inflammatory tissues in different degree which shows no significant change; there are respectively negative and unequally positive expressions in normal and inflammatory tissues. All these have proved that there are two kinds of isoenzyme expression in dental pulp, COX-2 and COX-1: COX-1 protein itself exists in cell, and continually produces PGs to sustain physiological need under normal condition; but COX-2 don't be detected in cell in normal physiological state, only if being stimulated by cytokines, it will be synthesized from the beginning, according to the course of DNA transcription into mRNA, then mRNA translation into protein, and at last AA metabolism into PGS. Presently, COX-2 can be synthesized by mesentery cell, monocular phagocyte, smooth muscle cell, vascular endothelial cell and fibroblast but no platelet. Feng and others found that COX-2 mRNA expression can be induced by endotoxin injected in body or stimulation of human umbilical vein endothelial cell with IL-1. Some scholar has also observed similar phenomena when stimulating vascular endothelial cell with TNF. Other studies show that hypoxia can induce sustained COX-2 expression, but COX-1 expression has no change. Recently, some learner finds that there are positive expressions of COX-2 in periodontal ligament and cementocyte during the course of inflammatory absorption of root of tooth. As far as pathophysiology is concerned, COX-1 has certain activity under normal condition to maintain body's physiological process, and keep homeostasis; COX-2 will be synthesized under the stimulation of pro-inflammatory cytokine; It is one of reason for inflammatory reaction.[26]In conclusion, endotoxin, inflammation medium, hypoxia environment and other damage factors can induce the synthesis of COX-2. Further...
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