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G Das Gupta

Publications and source records attributed to G Das Gupta.

8 recordsLinked to original sources
PubMed1991

Central muscarinic receptor subtypes and carrageenin-induced paw oedema in rats.

In an earlier report from this laboratory, it was demonstrated that the central cholinergic system exerted a modulatory pro-inflammatory effect on carrageenin-induced paw inflammation in rats. In this study, the role of the central muscarinic receptors in cholinergic modulation of peripheral inflammation was investigated by using several M1 and M2 receptor agonists and antagonists. The M1 receptor agonists aceclidine and arecholine and the nonspecific muscarinic receptor agonist oxotremorine augmented carrageenin oedema, an effect attenuated by the M1 receptor antagonist scopolamine. Physostigmine behaved like a M1 receptor agonist at all dose levels. However, the other M2 receptor agonist, carbachol, produced a dose-dependent dual effect, with lower doses attenuating the oedema and higher doses augmenting the inflammation. While the former action appeared to be due to M2 receptor stimulation, because it was blocked by AF-DX 116--a M2 receptor antagonist, the latter action appeared to be induced by M1 receptor stimulation, because it was inhibited by scopolamine. The pro-inflammatory effect of the M2 receptor antagonists AF-DX 116 and gallamine appeared to be induced by enhanced neuronal release of acetylcholine, because the effects were not evident following pretreatment with hemicholinium, which attenuates synthesis of the amine. Muscarinic receptor binding studies with (3H)-QNB indicated that the corpus striatum has substantially higher population of M1 receptors compared with the cerebellum. In the corpus striatum, (3H)-QNB binding indicated initial up-regulation followed by down-regulation of M1 receptors during peak inflammation, which appeared to persist even after a decrease in the inflammation. In contrast, the M1 receptors in the cerebellum appeared to be down-regulated very transiently during the early phase of the inflammation. While these receptor alterations may be due to the inflammation, it is equally possible that they represent changes induced by the stress of pain and inflammation induced by carrageenin.

Animals↗
PubMed1991

Antiulcerogenic and anti-inflammatory effects of emodin, isolated from Rhamnus triquerta wall.

Emodin, an anthraquinone derivative, isolated from the whole plant of R. triquerta, in 15 mg/kg dose (ip) exhibited anti-inflammatory activity against carrageenin-induced pedal inflammation in rats. In the same dosage it also showed antiulcer activity against 4 hr pylorus-ligated, aspirin and immobilization stress-induced gastric ulcers in rats. It decreased acid and pepsin output and augmented mucus secretion in terms of total carbohydrate: protein ratio in the gastric juice of aspirin treated pylorus-ligated rats, indicating that the antiulcerogenic effect of emodin may be due to its effect on gastric secretion.

Animals↗
PubMed1989

Effect of centrally administered prostaglandin D2 and some prostaglandin synthesis inhibitors on carrageenan-induced paw oedema in rats.

The putative modulatory role of central prostaglandins (PGs) on peripheral inflammation has been explored by investigating the effects of intracerebroventricularly (i.c.v.) administered PGD2, the major rodent brain PG, hydrocortisone, a phospholipase A2 inhibitor, and the cyclo-oxygenase inhibitors, paracetamol and mefenamic acid, on carrageenan-induced paw inflammation in rats. PGD2 produced a dose-related inflammation-augmenting effect, whereas hydrocortisone and the PG synthesis inhibitors, paracetamol and mefenamic acid, induced attenuation of the peripheral oedema. These findings confirm an earlier report from this laboratory which had indicated that central PGs may modulate peripheral inflammation and that conventional anti-inflammatory agents exert at least part of their effect by inhibiting central PG synthesis.

Acetaminophen↗
PubMed1988

Intracerebroventricularly administered bradykinin augments carrageenan-induced paw oedema in rats.

Intracerebroventricular (i.c.v.) administered bradykinin (2.5 and 5.0 micrograms/rat) was found to augment carrageenan-induced acute paw oedema throughout the 4 h post-carrageenan observation period. The effect was statistically significant with the higher dose. The pro-inflammatory effect of i.c.v. bradykinin was antagonized following pretreatment with hemicholinium and atropine ethoiodide administered i.c.v., drugs that reduce central cholinergic activity. Similarly, central administration of drugs that inhibit the synthesis of eicosanoids, hydrocortisone, diclofenac and paracetamol, also attenuated the pro-inflammatory effect of bradykinin. The findings indicate that the inflammation-promoting effect of centrally administered bradykinin involves the central prostaglandin and cholinergic neurotransmitter systems.

Animals↗
PubMedDate not supplied

Bioflavonoids and vasoactive mediator release from mast cells.

5-hydroxy and 7-hydroxy flavones significantly attenuated the carrageenin-induced pedal inflammation in rats; however, the anti-inflammatory effect declined at higher doses. These compounds produced positive inotropic effect on frog atria, which exhibited tachyphylaxis and was selectively abolished by indomethacin pretreatment. Studies on the rat mesenteric mast cells revealed that both the compounds, administered either in vitro or in vivo, induced a significant degree of mast cell degranulation in higher concentrations/doses. The mast cell degranulation induced by compound 48/80 was, however, prevented by lower, but not higher, concentrations/doses of the flavones. Local injection of 7-hydroxy flavone into the hind paw of rat showed that, in higher doses, the compound produced significant oedema. It was concluded that these compounds have a biphasic action: mast cell stabilisation and degranulation at lower and higher concentrations/doses, respectively.

Animals↗