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Hesperidin ameliorates heavy metal induced toxicity mediated by oxidative stress in brain of Wistar rats
Affiliation:1. Department of Anesthesiology, Far-Eastern Memorial Hospital, Pan-Chiao District, New Taipei City 22060, Taiwan;2. Graduate Institute of Basic Medicine, Fu Jen Catholic University, No. 510, Zhongzheng Rd., Xinzhuang Dist., New Taipei City 24205, Taiwan;3. School of Medicine, Fu Jen Catholic University, No. 510, Zhongzheng Rd., Xinzhuang Dist., New Taipei City 24205, Taiwan;4. Department of Clinical Psychology, Fu Jen Catholic University, No. 510, Zhongzheng Rd., Xinzhuang Dist., New Taipei City 24205, Taiwan;5. Department of Chemistry, Fu Jen Catholic University, No. 510, Zhongzheng Rd., Xinzhuang Dist., New Taipei City 24205, Taiwan;6. Department of Mechanical Engineering, Yuan Ze University, Taoyuan 320, Taiwan;1. Department of Pediatrics, University of Louisville School of Medicine, USA;2. Department of Bioinformatics and Biostatistics, University of Louisville School of Public Health and Information Sciences, USA;3. Department of Neurology, University of Louisville School of Medicine, USA;4. Department of Pharmacology and Toxicology, University of Louisville School of Medicine, USA;1. MOE, Key Laboratory of Cell Activities and Stress Adaptations, Lanzhou University, Lanzhou, 730000, Gansu Province, PR China;2. Department of Occupational and Environmental Health, School of Public Health, Lanzhou University, Lanzhou City, 730000, Gansu Province, PR China;1. Laboratory of Experimental Pathophysiology, Department of Biological Sciences and Center of Research in Biological Sciences, Federal University of Ouro Preto (UFOP), 35400-000, Ouro Preto, MG, Brazil;2. Laboratory of Immunobiology of Inflammation, Department of Biological Sciences, Institute of Exact and Biological Sciences, Federal University of Ouro Preto (UFOP), 35400-000, Ouro Preto, MG, Brazil;3. Laboratory of Neurobiology and Biomaterials, Department of Biological Sciences, Institute of Exact and Biological Sciences, Federal University of Ouro Preto (UFOP), 35400-000, Ouro Preto, MG, Brazil;4. Laboratory of Cardiovascular Physiology, Department of Biological Sciences and Center of Research in Biological Sciences, Federal University of Ouro Preto (UFOP), 35400-000, Ouro Preto, MG, Brazil;1. Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran;2. Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran
Abstract:Cadmium (Cd) induces neurotoxicity owing to its highly deleterious capacity to cross the blood brain barrier (BBB). Recent studies have provided insights on antioxidant properties of bioflavonoids which have emerged as potential therapeutic and nutraceutical agents. The aim of our study was to examine the hypothesis that hesperidin (HP) ameliorates oxidative stress and may have mitigatory effects in the extent of heavy metal-induced neurotoxicity. Cd (3 mg/kg body weight) was administered subcutaneously for 21 days while HP (40 mg/kg body weight) was administered orally once every day. The results of the current investigation demonstrate significant elevated levels of oxidative stress markers such as lipid peroxidation (LPO) and protein carbonyl (PC) along with significant depletion in the activity of non-enzymatic antioxidants like glutathione (GSH) and non-protein thiol (NP-SH) and enzymatic antioxidants in the Cd treated rats’ brain. Activity of neurotoxicity biomarkers such as acetylcholinesterase (AchE), monoamine oxidase (MAO) and total ATPase were also altered significantly and HP treatment significantly attenuated the altered levels of oxidative stress and neurotoxicity biomarkers while salvaging the antioxidant sentinels of cells to near normal levels thus exhibiting potent antioxidant and neuroprotective effects on the brain tissue against oxidative damage in Cd treated rodent model.
Keywords:Cadmium  Heavy metal  Hesperidin  Rats  Neurotoxicity  Antioxidant
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