Browsing by Author "S.U. Yanpallewar"
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PublicationArticle A preliminary study on the effect of Azadirachta indica on bronchial smooth muscles and mast cells(Natural Remedies Private Limited, 2003) S.B. Acharya; S.U. Yanpallewar; R.K. SinghObjective: The present study was designed to assess the protective effect of Azadirachta indica on bronchial smooth muscles and mast cells. Methods: Azadirachta indica (200 mg/kg p.o.) leaf juice was administered to animals and its protective effect was determined on histamine aerosol induced bronchospasm in guinea pigs, comp 48/80 induced mast cell degranulation and active anaphylaxis in rats. Results: A significant protection against histamine induced bronchospasm in guinea pigs was observed. There was 63% delay in onset of dyspnoea in A. indica treated animals against that of 16% in control animals. A. indica neither could prevent mast cell degranulation nor could protect against active anaphylaxis. Conclusion: The results of the present preliminary study reveal that A. indica has bronchoprotective role. Moreover, it also suggests that mechanisms other than that associated with mast cell degranulation or active anaphylaxis are possibly involved in bronchoprotective role of A.indica.PublicationArticle Effect of Azadirachta indica on paracetamol-induced hepatic damage in albino rats(Urban und Fischer Verlag Jena, 2003) S.U. Yanpallewar; S. Sen; S. Tapas; Mohan Kumar; S.S. Raju; S.B. AcharyaAzadirachta indica, a plant used widely in Ayurveda, has been reported to have anti-inflammatory, immunomodulatory and adaptogenic properties. The present study evaluates its hepatoprotective role. Fresh juice of tender leaves of Azadirachta indica (200 mg/kg body wt. p.o.) inhibited paracetamol (2 g/kg body wt. p.o.)-induced lipid peroxidation and prevented depletion of sulfhydryl groups in liver cells. There was an increase in serum marker enzymes of hepatic damage (aspartate transaminase, alanine transaminase and alkaline phosphatase) after paracetamol administration. Azadirachta indica pretreatment stabilized the serum levels of these enzymes. Histopathological observations of liver tissues corroborated these findings.PublicationArticle Evaluation of antioxidant and neuroprotective effect of Ocimum sanctum on transient cerebral ischemia and long-term cerebral hypoperfusion(2004) S.U. Yanpallewar; Sunita Rai; Mohan Kumar; S.B. AcharyaFree radicals are implicated in causation of cerebral reperfusion injury and chronic cerebral hypoperfusion in rats is associated with functional and histopathological disturbances. Ocimum sanctum (OS), a plant widely used in Ayurveda, has been shown to possess anti-inflammatory, antioxidant and cognition-enhancing properties. In the present study, we investigated the effect of methanolic extract of OS leaves in cerebral reperfusion injury as well as long-term hypoperfusion. Occlusion of bilateral common carotid arteries (BCCA) for 30 min followed by 45 min reperfusion caused increase in lipid peroxidation and up-regulation of superoxide dismutase (SOD) activity accompanied by fall in tissue total sulfhydryl groups (TSH) in rat forebrains. Ascorbic acid levels were unchanged, however. OS pretreatment (200 mg/kg/day for 7 days) prevented this reperfusion-induced rise in lipid peroxidation and SOD activity. OS pretreatment also stabilized the levels of TSH during reperfusion. Long-term cerebral hypoperfusion (a model of cerebrovascular insufficiency and dementia) induced by permanent occlusion of BCCA for 15 days demonstrated altered exploratory behavior in open-field testing and memory deficits as tested by Morris' water maze. Histopathological examination of hypoperfused animals revealed reactive changes, like cellular edema, gliosis and perivascular inflammatory infiltrate. OS treatment (200 mg/kg/day for 15 days) significantly prevented these hypoperfusion-induced functional and structural disturbances. The results suggest that OS may be useful in treatment of cerebral reperfusion injury and cerebrovascular insufficiency states. © 2004 Elsevier Inc. All rights reserved.PublicationArticle Nimodipine attenuates biochemical, behavioral and histopathological alterations induced by acute transient and long-term bilateral common carotid occlusion in rats(Academic Press, 2004) S.U. Yanpallewar; Debashish Hota; Sunita Rai; Mohan Kumar; S.B. AcharyaRestoration of blood flow to an ischemic brain region is associated with generation of reactive oxygen species with consequent reperfusion injury. Chronic cerebral hypoperfusion induced by permanent occlusion of bilateral common carotid arteries in rats is associated with behavioral and histopathological alterations. Nimodipine, a dihydropyridine calcium channel antagonist, has potent vasodilatory effect on cerebral vessels and increases cerebral blood flow. We analyzed whether nimodipine reduces injury caused by transient forebrain ischemia and long-term cerebral hypoperfusion. Bilateral common carotid occlusion for 30min followed by 45min reperfusion resulted in a two-fold increase in lipid peroxidation and superoxide dismutase activity. Nimodipine pretreatment (4mg/kg, i.p.) brought down these levels by 30 and 23%, respectively. Long-term cerebral hypoperfusion in rats caused a propensity towards anxiety and listlessness (open field paradigm) accompanied by deficits of learning and memory (Morris' water maze testing). Additionally, histopathological observation in hypoperfused brains revealed reactive changes in the form of perivascular inflammation, gliosis and astrocytosis. Nimodipine treatment significantly alleviated these changes in behavioral and histopathological parameters. Our data confirm the protective role of nimodipine in ischemia reperfusion injury. Moreover, it suggests the beneficial role of nimodipine in cerebrovascular insufficiency states and dementia. © 2003 Elsevier Ltd. All rights reserved.
