The effect of aqueous garlic extract on the levels of arachidonic acid metabolites (leukotriene C-4 and prostaglandin E(2)) in rat forebrain after ischemia-reperfusion injury


Batirel H. F. , Aktan S., Aykut C., Yegen B. , Coskun T.

PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS, cilt.54, sa.4, ss.289-292, 1996 (SCI İndekslerine Giren Dergi) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 54 Konu: 4
  • Basım Tarihi: 1996
  • Doi Numarası: 10.1016/s0952-3278(96)90061-7
  • Dergi Adı: PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS
  • Sayfa Sayıları: ss.289-292

Özet

Leukotriene C-4 (LTC(4)) and prostaglandin E(2) (PGE(2)) are known to be highly potent cerebral vasoconstrictors which are formed from arachidonic acid (AA). They enhance vascular permeability, inducing vasogenic edema that may damage the ischemic penumbra after ischemia and reperfusion. The inhibitory effect of aqueous garlic extract (AGE) on AA metabolism in human platelets is known. In this study, following the global ischemic model application to the rats, all underwent 10 min ischemia and were reperfused for different periods. The levels of LTC(4) and PGE(2) in rat forebrain were then measured. One rat group consisted of 8 rats. In the combined reperfused groups both metabolites increased significantly when compared with the 10 min ischemia alone, no reperfusion group (P < 0.05). In the 8 min reperfused group, PGE(2) and LTC(4) levels increased significantly at 60 min of reperfusion compared with each corresponding control group (P < 0.005). PGE, and LTC(4) levels were reduced significantly at 60 min of reperfusion compared with the 8 min reperfused group (P < 0.005). AGE (1 ml/kg) reduced both LTC(4) and PGE(2) levels significantly in the 8 min and 60 min reperfused group (P < 0.001, P < 0.001, P < 0.05, P < 0.01). In conclusion, AGE reduced LTC(4) and PGE(2) levels at a dosage of 1 ml/kg following 8 and 60 min reperfusion. It may be helpful in reducing AA metabolite levels and preventing injury after ischemic phenomena.