The dynamically changes of COX-2 and the gene expression of COX-2 mRNA after traumatic brain injury in rats / 法医学杂志

OBJECTIVE@#To illuminate the pathology of traumatic brain injury(TBI) and to better understand the relationship between the expression of COX-2 and the time course of TBI.@*METHODS@#Immunocytochemical staining, double-labeled with the anti-COX-2 antibody and either the neuron-specific antibody NeuN or the astroglial-specific marker GFAP, in situ hybridization and computer image analysis were used.@*RESULTS@#Results from immunohistochemistry indicated time-dependent staining changes of neuronal plasma. The immunostained cells were faint at control cortex, mostly were neurons. The immunostained cells appeared to be darkly stained 30 min after TBI for extended periods of time and reached the maximum at 2 d after injury, reached another peak (P < 0.05) at 4 d post-injury. The darker cells persisted in a high level, significant differences (P < 0.05) even presented between control and 15 d post-injury. The COX-2 mRNA expression was faint at control cortex. The expressions of COX-2 mRNA appeared to be darkly stained 15 min after TBI for extended periods of time and reached the maximum (P < 0.05) at 1 d post-injury, reached another peak (P < 0.05) at 3 d post-injury, and significant differences (P < 0.05) even presented between control and 7 d post-injury, but not 15 d post-injury.@*CONCLUSION@#The results of this study indicated that the expression of COX-2 mRNA and protein had a possible relationship with the extended periods of time after TBI. It might have some relationship between the expression of COX-2 and secondary brain injury after TBI.

Methyl-beta-cyclodextrin inhibits cell growth and cell cycle arrest via a prostaglandin E(2) independent pathway

Methyl-beta-cyclodextrin, a cyclic oligosaccharide known for its interaction with the plasma membrane induces several events in cells including cell growth and anti-tumor activity. In this study, we have investigated the possible role of cyclooxygenase 2 (COX-2) in cell growth arrest induced by methyl-beta-cyclodextrin in Raw264.7 macrophage cells. Methyl-beta-cyclodextrin inhibited cell growth and arrested the cell cycle, and this cell cycle arrest reduced the population of cells in the S phase, and concomitantly reduced cyclin A and D expressions. Methyl-beta-cyclodextrin in a dose- and time-dependent manner, also induced COX-2 expression, prostaglandin E(2) (PGE(2)) synthesis, and COX-2 promoter activity. Pretreatment of cells with NS398, a COX-2 specific inhibitor completely blocked PGE(2) synthesis induced by methyl-beta-cyclodextrin, however inhibition on cell proliferation and cell cycle arrest was not effected, suggesting non-association of COX-2 in the cell cycle arrest. These results suggest that methyl-beta-cyclodextrin induced cell growth inhibition and cell cycle arrest in Raw264.7 cells may be mediated by cyclin A and D1 expression.

Expression and significance of cyclooxygenase 2 gene in lung cancer / 华中科技大学学报（医学）（英德文版）

To study the expression of cyclooxygenase 2 (COX-2) gene and its relationship with clinicopathological characteristics of lung cancer, expression of the COX-2 mRNA was evaluated by reverse transcription polymerase chain reaction (RT-PCR) in cancerous tissues and paired adjacent non-cancerous tissues from 56 patients and benign lesions from 12 patients. Our results showed that expression of COX-2 gene was detected in a significantly greater proportion of cancerous tissues (60.7%) than adjacent noncancerous tissues (10.7%, P0.05). The up-regulation of COX-2 gene in lung cancer tissues especially in adenocarcinoma suggested that COX-2 may play a role in the lung carcinogenesis and COX-2 gene may serve as a potential therapeutic target in lung cancer.