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Naringin alleviates cognitive impairment,mitochondrial dysfunction and oxidative stress induced by d-galactose in mice
Authors:Anil Kumar  Atish PrakashSamrita Dogra
Affiliation:Pharmacology Division, University Institute of Pharmaceutical Sciences, UGC Centre for Advance Studies, Panjab University, Chandigarh 160014, India
Abstract:
Role of mitochondrial dysfunction and oxidative stress has been well documented in aging and related disorders such as Alzheimer’s disease. Bioflavonoids have been reported to have a therapeutic potential against several age related processes. Bioflavonoids are being used as a neuroprotectants in the treatment of various neurological disorders including aging. Therefore, present study has been conducted in order to explore the possible role of naringin against d-galactose induced cognitive dysfunction, oxidative damage and mitochondrial dysfunction in mice. Chronic administration of d-galactose (100 mg/kg) for 6 weeks significantly impaired cognitive performance (both in Morris water maze and elevated plus maze), locomotor activity, oxidative defense and mitochondrial complex (I, II and III) enzymes activities as compared to sham group. Six weeks naringin (40 and 80 mg/kg) treatment significantly improved cognitive performance, oxidative defense and restored mitochondria complex enzyme activities as compared to control (d-galactose). Naringin treatment significantly attenuated acetylcholine esterase activity in d-galactose treated mice. In conclusion, present study highlights the potential role of naringin against d-galactose induced cognitive impairment, biochemical and mitochondrial dysfunction in mice.
Keywords:ATP, adenosine triphosphate   ROS, reactive oxygen species   DNA, deoxyribonucleic acid   AGE, advanced glycation end products   RAGE, receptor for advanced glycation end products   IAL, initial acquisition latency   RL, retention latency   EGTA, ethylene glycol tetraacetic acid   HEPES, 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid   BSA, bovine serum albumin   SDH, succinate dehydrogenase   MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-H-tetrazolium bromide   MDA, malondialdehyde   DTNB, 5,5&prime  -dithio-bis (2-nitrobenzoic acid)   NBT, nitro blue tetrazolium   NOS, nitric oxide synthase   SOD, super oxide dismutase   TBARS, thiobarbituric acid reactive substances   6-OHDA, 6-hydroxydopamine   AChE, acetyl cholinesterase
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