oxidative stress.

The present study explored the neuroprotective role of d-Limonene in the cerebral ischemia-reperfusion injury in mice. Swiss Albino mice (either sex), weighing between 20-30 g were divided in different groups (n≥6). The animals were anaesthetized using Chloral hydrate (400 mg/kg; i.p.) and cerebral blood supply was occluded for 10 min and afterwards reperfusion for 24 h. d-Limonene has been administered in 3 doses (50, 100 and 200 mg/kg; p.o.) successively to mice for 30 days before surgery. Edaravone (3 mg/kg, i.p.) was used as standard drug. The effect of surgery on memory, anxiety, muscle relaxant and locomotor was estimated by using passive avoidance paradigm, elevated zero maze, rota rod apparatus, and actophotometer. After behavioural evaluation, the animals were sacrificed and brains were isolated, homogenized and centrifuged for TBARS, GSH, catalase and brain nitrite estimations. Ishemia-reperfusion injury caused decrease in locomotor, motor-co-ordination, decreased the time spent in open arm, no. of entries and increased in latency time in elevated zero maze and memory of mice. Ischemic mice showed higher brain TBARS and nitrite levels and lower GSH and catalase levels. However, d-Limonene administration significantly attenuated (p

Peucedanum grande has been found to be associated with the multiple therapeutic properties. In the present study, we have used P. grande as an ameliorating agent against nephrotoxic effects of Mercuric chloride (HgCl2). The rats were given pretreatment of P. grande orally at a dose of 60 and 120 mg/kg body weight for five consecutive days. Mercury chloride 4 mg/kg body .wt was used as renal toxicant, and injected subcutaneously in the neck region in a volume of 1 ml/kg. The modulatory effects of P. grande on HgCl2 induced nephrotoxicity was investigated by assaying oxidative stress biomarkers, lipid peroxidation, serum kidney toxicity markers and by histopathological examination of kidney. The HgCl2 induced nephrotoxicity by depleting antioxidant levels, elevating the level of serum creatinine and BUN, as well as damaging the normal architecture of kidney. P. grande pretreatment prevented deteriorative effects induced by HgCl2 through a protective mechanism that involved reduction of increased oxidative stress as well as by restoration of histopathological change against HgCl2 administration.