Neuroprotective efficacy of Nardostachys jatamansi and crocetin in conjunction with selenium in cognitive impairment

Oxidative stress leads to complex biochemical alterations, and has been implicated in the progressive loss of learning and memory. Supplementing and boosting the endogenous antioxidant defense system could impede the progression of various types of neurodegeneration. In the present study, we have investigated the neuroprotective efficacy of a low-dose combination of certain promising and powerful natural antioxidants in an experimental model of cognitive impairment.Combined pretreatmentwith the extract ofNardosatchys jatamansi (N), crocetin (C) and selenium(Se) as sodium selenite (N, 200 mg/kg + C, 25 μg/kg + Se, 0.05 mg/kg body weight) for 15 days led to improved behavioral outcomes in streptozotocin (STZ)-induced cognitive impairment in rats. While intracerebroventricular (ICV) infusion of STZ resulted in the significant elevation ofmarkers of oxidative stress and depletion of endogenous antioxidant defense system in the vehicle-pretreated group, these markers of oxidative stress and antioxidant enzymatic as well as nonenzymatic defense lines were attenuated in the group pretreated with the combination of antioxidants (NCSe). NCSe pretreatment markedly improved the performance of animals in passive avoidance test and Morris water maze (MWM) tasks, significantly reduced the level of TBARS, and elevated the content of glutathione and activities of antioxidant enzymes (glutathione peroxidase, glutathione-S-transferase and catalase).Our study reflects the synergistic potential of the above combination and concludes that amultimodal approach could be beneficial rather than a singular intervention. © Springer-Verlag 2012

Sesamin attenuates behavioral, biochemical and histological alterations induced by reversible middle cerebral artery occlusion in the rats

Restoration of blood flow to an ischemic brain region is associated with generation of reactive oxygen species (ROS) with consequent reperfusion injury. ROS cause lipid peroxidation, protein oxidation, and DNA damage, all of which are deleterious to cells. So diminishing the production of free radicals and scavenging them may be a successful therapeutic strategy for the protection of brain tissue in cerebral stroke. The present study investigated the neuroprotective effect of sesamin (Sn) to reduce brain injury after middle cerebral artery occlusion (MCAO). The middle cerebral artery (MCA) of adult male Wistar rat was occluded for 2 h and reperfused for 22 h. Sesamin is the most abundant lignan in sesame seed oil is a potent antioxidant. Sesamin (30 mg/kg) was given orally twice, 30 min before the onset of ischemia and 12 h after reperfusion. The initial investigations revealed that sesamin reduced the neurological deficits in terms of behavior and reduced the level of thiobarbituric acid reactive species (TBARS), and protein carbonyl (PC) in the different areas of the brain when compared with the MCAO group. A significantly depleted level of glutathione and its dependent enzymes (glutathione peroxidase [GPx] and glutathione reductase [GR]) in MCAO group were protected significantly in MCAO group treated with sesamin. The present study suggests that sesamin may be able to attenuate the ischemic cell death and plays a crucial role as a neuroprotectant in regulating levels of reactive oxygen species in the rat brain. Thus, sesamin may be a potential compound in stroke therapy. © 2009 Elsevier Ireland Ltd. All rights reserved