Life Sci 2010 Jun 28;86(25-26):928-35. Epub 2010 Apr 28.
Pharmacology Division, University Institute of Pharmaceutical Sciences, UGC Centre of Advanced Study, Panjab University, Chandigarh-160014, India.
Aim: The present study has been designed to explore the nitric oxide mechanism in the protective effect of naringin against I/R induced neurobehavioral alterations, oxidative damage and mitochondrial dysfunction in mice.
Main Methods: Laca mice (25-30 g) were subjected twice to BCCAO occlusion (5 min) at the interval of 10 min, followed by 96 h reperfusion. Naringin (50 and 100 mg/kg) was administered for 10 days, starting 7 days before the animals were subjected to I/R injury. On day 10, various neurobehavioral parameters followed by biochemical parameters and mitochondrial enzyme complex activities were assessed.
Key Findings: Ischemia reperfusion injury caused significant (increased immobility period, neurological score and decreased locomotor activity) oxidative damage (increased lipid peroxidation and nitrite concentration and depleted reduced glutathione, glutathione-S-transferase, superoxide dismutase and catalase) and altered mitochondrial enzyme complex activities (complex I to IV) as compared to sham treatment. Naringin (50 and 100 mg/kg) treatment significantly attenuated neurobehavioral alterations, oxidative damage and restored mitochondrial enzyme complex activities as compared to control (ischemia reperfusion) group. Further, protective effect of naringin (50 mg/kg) was attenuated by l-arginine (100 mg/kg) or sildenafil (5 mg/kg) pretreatment. Further, L-NAME (10 mg/kg) or 7-NI (10 mg/kg) pretreatment with naringin (50 mg/kg) significantly potentiated their protective effect as compared to their treatment alone.
Significance: The present study suggests the involvement of nitric oxide mechanism in the protective effect of naringin against post-stroke depression induced neurobehavioral, biochemical and cellular alterations in mice.