MDR 1 mRNA was also up regulated by celecoxib in U937 cells. Nevertheless, exactly the same analysis didn’t confirm any up regulation of the corresponding protein. These results suggest a differential capacity of COX 2 inhibitors to effect drug efflux and exclude that these two main multidrug resistance proteins are implicated. Altogether, these results exclude that drug efflux maybe the primary process accountable for the prevention of cell damage AG-1478 price caused by chemotherapeutic agents. To date, we’ve assessed an over-all ability of COX 2 inhibitors to combat stress induced apoptosis in U937 cells. We wanted to determine if this result was common. With this specific purpose, we extended our investigations to a section of hematopoietic cell lines, selecting origins, heterogeneous for COX 2 protein expression levels and different designs. Fig. 7B documents the consequences of nimesulide and celecoxib on apoptosis induced by cisplatin. Apoptosis was prevented by nimesulide in all the cell lines, with the exception of K562 cells. Apoptosis was always inhibited by celecoxib. These results verify that anti apoptotic potential of COX 2 inhibitors, moreover, taking a look at the differential quantities of COX 2 protein expression, it provides further evidence that COX 2 molecule is not implicated in this modulatory influence. In this research, we report that three different COX 2 inhibitors effectively fight the apoptogenic exercise of a broad screen of anti cancer agents, which are currently Inguinal canal used in centers. The effect especially worries compounds that trigger the intrinsic apoptotic signaling. In contrast, COX 2 inhibitors do not exert any modulatory effect on apoptosis induced by extracellular ligands. The implicit apoptotic cascade is inhibited at extremely early steps, ahead of Bax/Bak activation. More over, etoposide, used as an instrument to monitor the ability of chemotherapeutic agents to trigger cell injury, documents that COX 2 inhibitors strongly attenuate the generation of the apoptogenic anxiety. Our results show that COX 2 inhibitors affect only the experience of stress inducing agents. This isn’t the result of a modulation of the innate vs. extrinsic apoptotic pathways. We may only witness preventing the apoptotic signaling cascade without detecting any specific modifications of modulators AZD5363 of the intrinsic pathway, similarly. On the other hand, incredibly, the apoptogenic potential of H2O2, a typical stress that is triggered by a robust oxidative agent induced apoptosis, exactly as found for physical stimuli, is not affected by COX 2 inhibitors. The prevention of apoptosis is a true rescue from death and not only a of apoptotic signaling. DNA damage is indeed, prevented by cox 2 inhibitors, induced by etoposide.