Biomedical subjects

S T Reddy

Publications and source records attributed to S T Reddy.

39 records · Page 3Linked to original sources

PubMed1987

The accumulation of platelet activating factor in the injured cornea may be interrelated with the synthesis of lipoxygenase products.

The rabbit cornea accumulates platelet activating factor (PAF) three hrs after alkali burn. PAF was isolated by HPLC and assayed by platelet aggregation. This bioactivity was blocked by the PAF receptor antagonists BN 52021 and alprazolam. Added PAF increases the chemiluminescence response of the cornea in vitro and BN 52021 inhibits this effect. In vivo experiments show that the synthesis of 5-HETE and 12-HETE is inhibited by the PAF antagonist BN 52021. It is concluded that a metabolic interrelationship may exist between the PAF cycle and the lipoxygenation of arachidonic acid, and that drugs that affect these lipid mediators may modulate the inflammatory response of the anterior segment of the eye.

Alprazolam↗

PubMed1987

Inhibition of the alkali burn-induced lipoxygenation of arachidonic acid in the rabbit cornea in vivo by a platelet activating factor antagonist.

We have evaluated the involvement of 1-0-alkyl-2-acetyl-sn-glycero-3-phosphocholine (platelet activating factor, PAF), a membrane derived lipid mediator, in the inflammatory response of the anterior segment of the rabbit eye after corneal injury. The action of BN 52021, an antagonist of PAF receptor, was tested in vivo in models of corneal injury by alkali burn. The sodium salt of 1-14C-arachidonic acid was injected in the anterior chamber and the production of labeled prostaglandins and hydroxyeicosatetraenoic acid (HETE) was monitored as an index of the activation of the cyclooxygenase and lipoxygenase pathways. Topically applied BN 52021 produced a specific inhibition of the formation of labeled 5- and 12-HETE. This inhibition was maximal when the drug was applied during the first few hours after the injury. The drug does not affect the increased protein concentration in the aqueous humor after injury. These results suggest involvement of PAF in the inflammatory response in the cornea that could be blocked by the antagonist.

Alkalies↗

PubMed1987

Calcium- and phospholipid-dependent protein kinase C and phosphatidylinositol kinase: two major phosphorylation systems in the cornea.

The signaling messengers for the regulation of intracellular calcium-dependent functions involve a phospholipid-sensitive protein kinase (protein kinase C) modulated by diacylglycerol, which is a product of phosphoinositide degradation. We found that protein kinase C activity is two times higher in the epithelium than in the stroma-endothelial layers of the rabbit cornea. 12-0-tetradecanoylphorbol-13-acetate (TPA) and phosphatidylserine stimulate protein kinase C at low Ca2+ concentrations. The TPA-phosphatidylserine stimulated activity of corneal epithelium was recovered in the soluble fraction; in the membrane-bound fraction, a very active phosphatidylinositol kinase accounted for half the basal phosphorylation of the corneal epithelium.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗