Objective: To determine whether 17-a hydroxyprogesterone (17-OHPC) alters tumor necrosis factor-a (TNF-a) production and the expression of cyclooxygenase type 2 (COX-2) in myometrium exposed to lipopolysaccharide (LPS).Study Design: Lower segment myometrial biopsies were obtained from non-laboring patients at term. Tissues were cultured in serum-free media with 17-OHPC (1 mM) and LPS (1 mg/ml), either alone or in combination. At 24 h, the production of tumor necrosis factor-a (TNF-a) and the expression of COX-2 was determined using enzyme linked immunosorbent assay and real-time (RT-PCR). Statistical analysis was performed using non-parametric testing. A P-value of <0.05 was considered significant.Result: 17-OHPC had no effect on TNF-a production and COX-2 expression when compared with untreated myometrial explants (P ¼ 0.61 and P ¼ 0.95). LPS induced production of TNF-a (P ¼ 0.03) and expression of COX-2 (P ¼ 0.02). Treatment with 17-OHPC did not block LPS-induced TNF-a production (P ¼ 0.37) or COX-2 expression (P ¼ 0.12).
Conclusion:In this pilot study, 17-OHPC did not affect the production of TNF-a or COX-2 expression in human myometrium.
It has been demonstrated that lysolecithin (lysophosphatidyl choline, LPC) produces experimental cholecystitis in cats mediated by arachidonic acid metabolites. LPC is a cytolytic agent that has been postulated as a contributing factor in the development of cholecystitis in humans. The purpose of this research was to evaluate the effect of LPC on human gall-bladder mucosal cell phospholipase A2 and cyclooxygenase activity. Gall-bladder mucosal cells were isolated from the gall-bladders of patients undergoing routine cholecystectomy. Fresh, isolated cells were maintained in tissue culture and stimulated with varying doses of LPC. Platelet-activating factor concentration was quantitated as an index of phospholipase A2 activity and prostanoids were measured as an index of cyclooxygenase activity. Also, the effect of LPC on cyclooxygenase 1 and 2 expression in microsomal protein was evaluated. LPC caused dose related increases in 6-keto-PGF1α and PAF produced by human gall-bladder mucosal cells. Exposure of human gall-bladder mucosal cells to LPC failed to elicit expression of constitutive cyclooxygenase-1, while the expression of inducible cyclooxygenase-2 was increased. The results of this study indicate that LPC induces the formation of prostanoids and PAF by human gall-bladder mucosal cells, suggesting that this substance may promote the development of gall-bladder inflammation.
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