Investigation of COX and signaling pathways involved in human platelet

Abstract: In the present study, the mechanism(s) of synergistic interaction of various platelet mediators such as arachidonic acid (AA) when combined with 5-hydroxytryptamine (5-HT) or adenosine diphosphate (ADP) on human platelet aggregation were examined. Read this original research and sign up to receive Drug Design, Development and Therapy journal here: http://www.dovepress.com/articles.php?article_id=22478
Figure 1 Cascade of metabolism of arachidonic acid by COX pathways.

Figure 1 Cascade of metabolism of arachidonic acid by COX pathways.

Figure 2 GPCR s signaling networks in human platelets. 5-HT receptor blockers (a): cyproheptadine and ketanserin.

Figure 2 GPCR s signaling networks in human platelets. receptor blockers (a): cyproheptadine and ketanserin.

Figure 6 Tracings from representative experiments showing (A) concentration-dependent effect of AA , (B) concentration-dependent effect of ADP, (C) synergistic effect of AA (0.2 mmol/L) and ADP (0.5 μmol/L) on human platelet aggregation. Control = (ADP + AA ), n=5.

Figure 6 Tracings from representative experiments showing (A) concentration-dependent effect of AA , (B) concentration-dependent effect of ADP, (C) synergistic effect of AA mmol/L) and ADP μmol/L) on human platelet aggregation.

Figure 7 Tracings from representative experiments showing the synergistic effect of ADP [0.5 μmol/L] and AA [0.2 mmol/L] on human platelet aggregation is blocked by COX inhibitors, (A) ibuprofen and (B) celecoxib; (C) phospholipase C inhibitor, U73122; and (D) MAPK inhibitor, PD98059. Control = (ADP + AA ), n=5.

Figure 7 Tracings from representative experiments showing the synergistic effect of ADP [0.5 μmol/L] and AA [0.2 mmol/L] on human platelet aggregation is blocked by COX inhibitors, (A) ibuprofen and (B) celecoxib; (C) phospholipase C inhibitor, U73122; and (D) MAPK inhibitor, PD98059. Control = (ADP + AA ), n=5.

Figure 3 Tracings from representative experiments showing (A) concentration-dependent effect of 5-HT, (B) concentration-dependent effect of AA , (C) synergistic effect of AA (0.2 mmol/L) and 5-HT (5 μmol/L) on human platelet aggregation, n=5.

Figure 3 Tracings from representative experiments showing (A) concentration-dependent effect of (B) concentration-dependent effect of AA , (C) synergistic effect of AA mmol/L) and μmol/L) on human platelet aggregation,

Figure 4 Tracings from representative experiments showing the synergistic effect of 5-HT (5 μmol/L) and AA (0.2 mmol/L) on human platelet aggregation is blocked by COX inhibitors, (A) ibuprofen and (B) celecoxib; (C) phospholipase C inhibitor, U73122; and (D) MAPK inhibitor, PD98059. Control = (5-HT + AA ), n=5.

Figure 4 Tracings from representative experiments showing the synergistic effect of 5-HT (5 μmol/L) and AA (0.2 mmol/L) on human platelet aggregation is blocked by COX inhibitors, (A) ibuprofen and (B) celecoxib; (C) phospholipase C inhibitor, U73122; and (D) MAPK inhibitor, PD98059. Control = (5-HT + AA ), n=5.

Figure 5 Tracings from representative experiments showing the synergistic effect of 5-HT (5 μmol/L) and AA (0.2 mmol/L) on human platelet aggregation is blocked by 5-HT2 receptor blockers such as (A) cyproheptadine and (B) ketanserin. Control = (5-HT + AA ), n=5.

Figure 5 Tracings from representative experiments showing the synergistic effect of μmol/L) and AA mmol/L) on human platelet aggregation is blocked by receptor blockers such as (A) cyproheptadine and (B) ketanserin.

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