title: Quercetin protects against acute immobilization stress-induced behaviors and biochemical alterations in mice.
abstract: Oxidative stress is a major contributor to the alterations of various pathological conditions, including neurodegenerative and neuropsychiatric problems. Antioxidative flavonoids, ubiquitously included in vegetables, fruits, and teas, are expected to prevent degenerative diseases. Recently, flavonoids have been characterized as neuroprotectants in the treatment of various neurological disorders. The present study was designed to investigate protective effects of quercetin, a bioflavonoid, against acute immobilization-induced behavioral and biochemical alterations in mice. Mice were immobilized for a period of 6 hours. Quercetin (20 and 40 mg/kg, i.p.) was administered 30 minutes before subjecting the animals to acute stress. Behavioral tests (mirror chamber, actophotometer, and tail flick test) and biochemical analysis (malondialdehyde, reduced glutathione, catalase, nitrite, and protein levels) were subsequently performed. Acute immobilization stress for a period of 6 hours caused severe anxiety, analgesia, and impaired motor activity in mice. Biochemical analyses revealed an increase in malondialdehyde and nitrite levels as well as partial depletion of reduced glutathione and catalase activity in immobilization-stressed brain. Behavioral and biochemical parameters were significantly altered as compared to naive mice. Pretreatment with quercetin (20 and 40 mg/kg, i.p.) significantly reversed immobilized stress-induced anxiety and analgesia and reduced locomotor activity. Biochemically, quercetin treatment attenuated malondialdehyde accumulation and nitrite activity and restored the depleted reduced glutathione and catalase activity. Neuroprotective effects of quercetin were significantly improved as compared to control (immobilized stressed) animals. Results suggest that neuroprotective properties of quercetin can be used in the treatment and management of stress and related disorders.
authors.affiliation: Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh, India. kumaruips@yahoo.com
authors.forename: Anil
authors.initials: A
authors.lastname: Kumar
authors.forename: Richa
authors.initials: R
authors.lastname: Goyal
mesh_terms: D000818:Animals; D001007:Anxiety / Q000188:drug therapy; D001522:Behavior, Animal / Q000187:drug effects*; D002374:Catalase / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D007103:Immobilization; D015227:Lipid Peroxidation; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D009043:Motor Activity / Q000187:drug effects; D009422:Nervous System Diseases / Q000188:drug therapy*; D009569:Nitric Oxide / Q000378:metabolism; D009573:Nitrites / Q000378:metabolism; D018384:Oxidative Stress; D017288:Pain Threshold / Q000187:drug effects; D020011:Protective Agents / Q000494:pharmacology* / Q000627:therapeutic use; D011794:Quercetin / Q000494:pharmacology* / Q000627:therapeutic use; D013312:Stress, Physiological
chemical_list: D009573:Nitrites; D020011:Protective Agents; D009569:Nitric Oxide; D008315:Malondialdehyde; D011794:Quercetin; D002374:Catalase; D005978:Glutathione