# Immunomodulatory Effects of Pentoxifylline: Profiling Data Based on RAW 264.7 Cellular Signaling
## 3 Results
However, it is presumed that inhibition of these markers may reduce the T-cell mediated inflammatory response, thereby regulating the immune response. PTX can affect immunity-related proteins and, in turn, inhibit T-cell-associated immunity (Figure 4b). **Expression of p53-mediated apoptosis-related proteins**. Significantly reduced p53 expression (86.4%) with a concurrent decrease in MDM2 expression (85.1%) and PARP (92.2%)--but it increased p53-mediated apoptosis-related proteins, such as BAX (111.1%) and APAF-1 (106.3%)--was found. The expression levels of BAK (96.6%) and caspase 9 (97.5%) proteins showed slight decreases with time but were similar to housekeeping proteins within 5%. These results suggest that PTX significantly inhibited p53 but did not show any significant changes in down-regulated proteins (Figure 5a). Figure 4: (**a**) Changes to immunity and inflammation-upregulated proteins after PTX treatment in RAW 264.7 cells. Left-sided graph shows changes to protein expression according to the application time of PTX, blue bar; control group, red bar; 12 h treatment of PTX, green bar; 24 h treatment of PTX, purple bar; 48 h treatment of PTX. Right-sided polygonal graph shows protein expression profiles after 12 h treatment of PTX. (**b**) Changes to immunity and inflammation down-regulated proteins after PTX treatment in RAW 264.7 cells. Left-sided line graft shows changes to protein expressions after PTX treatment over time. Right-sided polygonal graph shows protein expression profiles after 12 h treatment of PTX. Figure 5: (**a**) Changes to p53 mediated apoptosis-related proteins after PTX treatment in RAW 264.7 cells; (**b**) changes to FAS-mediated apoptosis-related proteins after PTX treatment in RAW 264.7 cells. Left-sided graph shows changes to protein expression according to the application time of PTX, blue bar; control group, red bar; 12 h treatment of PTX, green bar; 24 h treatment of PTX, purple bar; 48 h treatment of PTX. Right-sided polygonal graph shows protein expression profiles after 12 h treatment of PTX. **Expression of F-mediated apoptosis-related proteins**. A decreased expression of FASL (90.9%), FADD (84.8%), and FLIP (88.7%) is shown. Caspase 8 expression levels were consistently down-regulated by PTX to 89.0% of baseline. The expression of FAS (95.6%) showed only a slight change but was within 5% of the control housekeeping proteins. The expression of PARP slightly decreased to 92.2% by PTX. These results suggested that PTX tends to inhibit FAS-mediated cell death (Figure 5b). **Expression of cell protection-related proteins**. A significant induction of some types of cytoprotective proteins: HSP-70 (110.2%), AP-1 (111.3%), SP-1 (113.4%), and PKC (105.1%) was observed. The expression levels of HSP-90 (93.2%) slightly decreased in 24-hour-treated cells; however, they were increased in the samples treated for 48 h. In the PTX treatment group, p38 (84.4% in the 12-h-treated sample), pAKT (89.1%), TERT (93.7%), and SP-3 (88.9%) were significantly decreased. JNK-1 showed minimal changes of less than \(\pm\)5% after PTX treatment (Figure 6a). These findings suggest that the cytoprotective effect increased up to 12 h but was down-regulated as time progressed. Figure 6: (**a**) Changes to cellular protection and survival-related proteins after PTX treatment in RAW 264.7 cells; (**b**) changes to antioxidant-related proteins after PTX treatment in RAW 264.7 cells; (**c**) changes to angiogenesis-related proteins in after PTX treatment in RAW 264.7 cells. Left-sided graph shows changes to protein expressions according to the application time of PTX, blue bar; control group, red bar; 12 h treatment of PTX, green bar; 24 h treatment of PTX, purple bar; 48 h treatment of PTX. Right-sided polygonal graph shows protein expression profiles after 12 h treatment of PTX. **Expression of antioxidant-related proteins**.