Centrophenoxine benefit a nootropic product
July 2 2016

Neurochemistry International. 2009. Effect of centrophenoxine against rotenone-induced oxidative stress in an animal model of Parkinson's disease. Oxidative stress has been implicated in the etiology of Parkinson's disease (PD). The important biochemical features of PD, being profound deficit in dopamine (DA) content, reduced glutathione (GSH), and enhanced lipid peroxidation (LPO) in dopaminergic (DA-ergic) neurons resulting in oxidative stress, mitochondrial dysfunction and apoptosis. Rotenone-induced neurotoxicity is a well acknowledged preclinical model for studying PD in rodents as it produces selective DA-ergic neuronal degeneration. In our previous study, we have shown that chronic administration of rotenone to rats is able to produce motor dysfunction, which increases progressively with rotenone treatment and centrophenoxine (CPH) co-treatment is able to attenuate these motor defects. The present study was carried out to evaluate the antioxidant potential of CPH against rotenone-induced oxidative stress. Chronic administration of rotenone to SD rats resulted in marked oxidative damage in the midbrain region compared to other regions of the brain and CPH co-treatment successfully attenuated most of these changes. CPH significantly attenuated rotenone-induced depletion in DA, GSH and increase in LPO levels. In addition, the drug prevented the increase in nitric oxide (NO) and citrulline levels and also enhanced the activity of catalase and superoxide dismutase (SOD). Histological analysis carried out using hematoxylin and eosin staining has indicated severe damage to mid brain in comparison to cortex and cerebellum and this damage is attenuated by CPH co-treatment. Our results strongly indicate the possible therapeutic potential of centrophenoxine as an antioxidant in Parkinson's disease and other movement disorders where oxidative stress is a key player in the disease process.

Brain Research. 2008. Behavioral alterations in rotenone model of Parkinson's disease: attenuation by co-treatment of centrophenoxine. Rotenone, a potent specific inhibitor of mitochondrial complex-1, appears to reproduce the behavioral features of Parkinson's disease in rats. It destroys dopaminergic neurons selectively, causing deficiency of dopamine in striatum which leads to impaired motor functions. Oxidative stress generated as a result of mitochondrial dysfunction and metabolism of dopamine has been implicated as an important factor in the etiology of Parkinson's disease. Present study explores the potential of centrophenoxine (a well known anti-aging and antioxidant drug) against rotenone induced motor dysfunction. Sprague Dawley male rats were administered with rotenone on a daily basis by subcutaneous injection of dose: 2 mg/kg body weight over a period of 35 days. Data showed impaired motor function, significant increase in catalepsy, decrease in locomotor activity and decrease in muscle activity. Dopamine content of rotenone treated animals was found to decrease significantly and lipid peroxidation was found to increase significantly in rotenone treated animals when compared with co-treated group. Co-treatment with centrophenoxine (100 mg/kg i.p. for 35 days) significantly attenuated the extent of motor dysfunction and changes in the level of dopamine and lipid peroxidation induced by rotenone toxicity. Thus, the present study provides evidence that centrophenoxine co-treatment attenuates rotenone induced motor dysfunction by virtue of its antioxidant action.

Molecular and Cellular Biochemistry. 2006. Evidence for centrophenoxine as a protective drug in aluminium induced behavioral and biochemical alteration in rat brain. Potential use of various nootropic drugs have been a burning area of research on account of various physical and chemical insult in brain under different toxicological conditions. One of the nootropic drug centrophenoxine, also known as an anti-aging drug has been exploited in the present experiment under aluminium toxic conditions. Aluminium was administered by oral gavage at a dose level of 100 mg/Kg x b x wt/day for a period of six weeks. To elucidate the region specific response, study was carried out in two different regions of brain namely cerebrum and cerebellum. Following aluminium exposure, a significant decrease in the activities of enzymes namely Hexokinase, Lactate dehydrogenase, Succinate dehydrogenase, Mg(2+) dependent ATPase was observed in both the regions. Moreover, the activity of acetylcholinesterase was also reported to be significantly decreased. Post-treatment with centrophenoxine was able to restore the altered enzyme activities and the effect was observed in both the regions of brain although the activity of lactate dehydrogenase and acetylcholinesterase did not register significant increase in the cerebellum region. Further, centrophenoxine was able to improve the altered short-term memory and cognitive performance resulted from aluminium exposure. From the present study, it can be concluded that centrophenoxine has a potential and can be exploited in other toxicological conditions also.

Exp Gerontol. 2005. Modulatory effects of centrophenoxine on different regions of ageing rat brain. The debilitating consequences of age-related brain deterioration are widespread and extremely costly in terms of quality of life and longevity. Free radical induced damage is thought to be responsible, at least in part, for the degenerative effects of aging. This may be largely due to high-energy requirements, high oxygen consumption, high tissue concentration of iron and low of antioxidant enzymes in brain. Therefore, supplementing an external source of free radical scavenger would greatly benefit in ameliorating the free radical damage which may thus be beneficial in aging. In the present study, an important nootropic agent Centrophenoxine, which has an easy access to brain, has been administered to aged animals (16 months old). Rats aged 6 months (young group) and 16 months old (old group) were chosen for the study. Both groups were administered Centrophenoxine (dissolved in physiological saline) intraperitoneally once a day for 6 weeks. Our study indicates an increased activity of Catalase, Superoxide Dismutase, Glutathione reductase, as well as an increase in the reduced, oxidized, and total glutathione content thus resulting in an altered redox state. A substantial increase in the malondialdehyde content was also reported as a result of aging. Whereas, following Centrophenoxine administration (100 mg/kg body weight/day, injected i.p) alterations in the activities of Superoxide dismutase, Glutathione reductase as well as in the reduced and oxidized glutathione content was reported in aged rat brain. Lipid peroxidation was also reported to be significantly decreased in aged animals after Centrophenoxine supplementation for 6 weeks. The use of an extraneous antioxidant substance may prove beneficial in combating the conditions of oxidative stress in ageing brain.