| Nonsteroidal anti-inflammatory drugs (NSAIDs) are a kind of inhibitor of cyclooxygenase(COX). COX is a key and rate-limited enzyme in aracidonate metabolism .Two COX isomers were found so far ,COX-1 and COX-2. COX-1 is a constitutive protein in normal cell and involves in synthesis of prostaglandins and homeostasis of various physiologic functions as a physiologic gate-keeper. On contrast, the COX-2 usually expresses none or very little in normal tissues, which only expresses by inducible stimulation. Recently research find that COX-2 expresses highly in tumor tissues or precancerous lesion tissues, which suggests that COX-2 relates to tumor close. Epidemiology and experiment study find NSAIDs, especially selective COX-2 inhibitor can inhibit tumorgenesis. For example, chronic intake of aspirin or other NSAIDs over a 10- to 15- year period resulted in approximately a 40%-50% reduction in the relative risk of developing colon cancer, hi gastric cancer, breast cancer, prostate cancer, ovary cancer and so on all demonstrates the similar results.There are very few studys of NSAIDs on bladder tumor .A animal model study found celecoxib could inhibit bladder tumor growth. However,Whether the COX-2 selective inhibitor or non COX-2 selective are more efficacy in inhibiting tumorgenesis, and whether NSAIDs can increase the effect ofchemotherapy can't be found . So we investigate the effect of the non-COX2 selective inhibitor indomethacin (IN) and COX-2 selective inhibitor celecoxib and they co-incubated with mitomycin on bladder tumor cell line T24.Methods 1,MTT assaysThe bladder tumor cell line T24 were treated with IN (50uM, lOOuM, 200uM, 400uM, 800uM)> celecoxib (25uM,50uM, lOOuM, 200uM, 400uM) and DMSO(0.4%), after 12hours, 24hours, 48hour, 72hour, the cell growth inhibition rate were measured. We also studied the bladder tumor cell line treated with IN (50uM, 200uM, SOOuM) and celecoxib (25uM, lOOuM, 400uM) co-incubation with MMC(2.5ug/ml) in 48hours.2, Flow cytometry assaysThe bladder tumor cell line T24 were treat with IN (50uM, 200uM, SOOuM) or celecoxib (25uM, lOOuM, 400uM), after 2hours, 12hours, 24hours, the apoptosis rate were studied.3, AO/EB fluorescence microscopy assaysWe also observed the apoptosis of bladder tumor cell line T24 after 24hours treating with IN (50uM, 200uM, SOOuM) by AO/EB fluorescence microscopy assays.Results1, The growth inhibition Effect of IN and celecoxib on T24 cell by MTT assay1,1 The effect of IN: IN couldn't inhibit the T24 cell growth at 50uM,but could inhibit 32.17%?.97%(P<0.05) cell growth at 200uM after 72 hours treatment. The growth inhibition rate became 47.82% + 2.48%(P<0.05) after treating with SOOuM in 24 hours, and increased to 85.43%?.09% (P<0.05)after treating with 72 hours. The 0.4% DMSO hadno effect on cell line (P>0.05) .1.2 The effect of celecoxib: Celecoxib could inhibit cell growth at 25uM after treating with 12 hours(cell growth inhibition rate was 5.90%?.69% P<0.05).At 50uM .celecoxib could inhibit 22.38% ?.66% cell growth after treating wilh 24 hours, and became 31.76%?1.84% after 72 hours(P<0.05).1.3 Compare the effect of IN with celecoxib's at same concentration: The anti-tumorgenesis effect of celecoxib was more efficacy than IN'sat same concentration, the cell growth inhibition differential value between two drugs was 27.68% ?.06% at 50 u M after treating with 72 hours, and the value became 6.37%?.02% at 400 uM after treating with the same time (P<0.05). 2,BV and celecoxib could increase the chemotherapy effect of MMC:2.1 The T24 cell growth inhibition was 20.28% ?1.97% > 0.02% ?2.19%> 77.11%?.55% respectively when treated with MMC (2.5 u g/MLX 50 U M IN or 200 U M IN alone. If MMC combined with 50 u M or 200 11 M IN, the cell growth inhibition rate increase to 26.81%?.70% (PO.05X 87.5%?.76% (P<0.05) respectively.2.2 When treated with celecoxib at 25 H M 100 U M 400 U M alone,the T24 cell trowth inhibition was 11.8%?.63%> 33.58%?.20%> 53.87%?4.50% respectively. If MMC combined with celec...
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