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Articles by S.A. Saeed
Total Records ( 3 ) for S.A. Saeed
  S.A. Saeed , H. Rasheed , T.M. Ali , Y. Qazi , S. Kabraji , L. Paul , R. Khan , F.A. Hussain and S. Ahmad
  This study was conducted to investigate the effects of nimesulide in platelet aggregation. It shows that nimesulide (1-100 μ M) inhibited platelets aggregation induced by adrenaline, (20-200 μ M). It also inhibed thromboxane A2 (TXA2) formation by platelets at low concentration (IC50; 1 μ M). However, much lower concentrations of nimesulide (0.01-0.1 μ M) potentiated the aggregatory response of subthreshold concentrations of adrenaline (0.2-2 μ M). Such an effect was blocked by Ca2+-channel blockers, verapamil and diltiazem (IC50: 7 and 46 μ M, respectively), nitric oxide donor, SNAP (IC50: 2 μ M) and cinchonine (10 nM) but not by genistein (up to 10 μ M). These results are indicative of the concentration-dependent dual effects of nimesulide on human platelet aggregation. The synergistic effect of low doses of nimesulide and adrenaline seems to be mediated through inhibition of multiple signaling pathways.
  K.H. Janbaz , S.A. Saeed and A.H. Gilani
  The hepatoprotective activity of thymol, a terpenoid from essential oils of plant origin was investigated against paracetamol and CCl4-induced hepatic damage. The results showed that paracetamol produced 100% mortality at the dose of 1 g kg 1 in mice while pre-treatment of animals with thymol (150 mg kg-1) reduced the death rate to 30%. Oral administration of paracetamol (640 mg kg-1) produced liver damage in rats as manifested by the rise in serum enzyme levels of alkaline phosphatase (ALP) and transaminases (AST and ALT). Pre-treatment of rats with thymol (150 mg kg-1) prevented the paracetamol-induced rise in serum enzymes. The hepatotoxic dose of CCl4 (1.5 ml kg-1; orally) also raised the serum ALP, AST and ALT levels. The same dose of thymol (150 mg kg-1) was able to prevent the CCl4-induced rise in serum enzymes. The results indicated that thymol also prevented the CCl4-induced prolongation in pentobarbital sleeping time confirming hepatoprotectivity. It was concluded that thymol possesses anti-hepatotoxic activity.
  S.A. Saeed , H. Rasheed , S. Kumar , T.M. Ali , M.U. Butt , R.Dhangana , A. Jafri , S. Zehra and A.H. Gilani
  This study was conducted to examine the mechanism(s) of synergistic interaction of platelet-activating factor (PAF) and arachidonic acid (AA) in platelet aggregation. We found that the synergism in platelet aggregation mediated by subthershold concentration of PAF (5-40 nM) and AA (0.1-0.2mM) was inhibited by PAF receptor blocker (WEB 2086, IC50= 0.6 然) showing that the effect is receptor mediated. To examine the role of the downstream signaling pathways, we found that such an interaction was inhibited by calcium channel blockers, diltiazem (IC50= 15 然) and verapamil (IC50 = 20 然), as well as by low concentrations of phospholipase C (PLC) inhibitor (U73122; IC50 = 6 然) and MAP kinase inhibitor, PD 98059 (IC50= 3.5 然). Inhibitor of AA-cyclooxygenase (flurbiprofen: IC50 = 3 然) also inhibited PAF and AA induced aggregation showing the involvement of COX pathway. On the other hand, herbimycin A, a specific inhibitor of tyrosine light chain kinase (TLCK) and SNAP, a nitric oxide (NO) donor also inhibited PAF and AA-induced aggregation with IC50 values of 15 and 1.7 然 respectively. However, the inhibitor of protein kinase C (chelerythrine; 20 然)) had no effect on aggregation induced by PAF and AA. These data suggest that the synergism between PAF and AA in platelet aggregation involves activation of PLC, COX, MAP kinase, TLCK and NO signaling pathways.
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