title: Carvacrol attenuates diabetes-associated cognitive deficits in rats.
abstract: Carvacrol (CAR), a naturally occurring phenolic monoterpene, has been demonstrated to possess various biological actions. The present study was designed to investigate the neuroprotective effect of CAR on diabetes-associated cognitive deficit (DACD) in a rat model of diabetes and exploring its potential molecular mechanism. Diabetic rats were treated with CAR by the doses of 25, 50, and 100 mg/kg for 7 weeks. Morris water maze was used for behavioral evaluation of memory. Cytoplasmic and nuclear fractions of cerebral cortex and hippocampus were prepared for the quantification of oxidative stress (MDA, SOD, and GSH), NF-κB p65 unit, TNF-α, IL-1β, and caspase-3. After 7 weeks of streptozotocin injection, the rats produced remarkable increase in escape latency, coupled with increased oxidative stress (increased MDA level and decreased SOD as well as reduced GSH), NF-κB p65 unit, TNF-α, IL-1β, and caspase-3 in different regions of diabetic rat brain. Interestingly, coadministration of CAR significantly and dose-dependently prevented behavioral, biochemical, and molecular changes associated with diabetes. In summary, our findings provide the first evidence that CAR can remarkably attenuate DACD and suggest the involvement of oxidative stress, inflammation, and apoptotic cascades in the development of cognitive impairment caused by diabetes. The pharmacological effect of CAR suggests that it may be used as a promising agent for the treatment of conventional antihyperglycemic regiments as well as DACD.
authors.affiliation: Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, China.
authors.forename: Wenjing
authors.initials: W
authors.lastname: Deng
authors.forename: Hong
authors.initials: H
authors.lastname: Lu
authors.forename: Junfang
authors.initials: J
authors.lastname: Teng
mesh_terms: D000818:Animals; D053148:Caspase 3 / Q000235:genetics / Q000378:metabolism; D002540:Cerebral Cortex / Q000378:metabolism / Q000503:physiopathology; D003072:Cognition Disorders / Q000188:drug therapy* / Q000209:etiology; D000081007:Cymenes; D003921:Diabetes Mellitus, Experimental / Q000150:complications*; D006624:Hippocampus / Q000378:metabolism / Q000503:physiopathology; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D008297:Male; D018782:Maze Learning; D039821:Monoterpenes / Q000008:administration & dosage / Q000627:therapeutic use*; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar; D051996:Transcription Factor RelA / Q000235:genetics / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D000081007:Cymenes; D053583:Interleukin-1beta; D039821:Monoterpenes; D051996:Transcription Factor RelA; D014409:Tumor Necrosis Factor-alpha; C073316:carvacrol; D053148:Caspase 3